STUDY - Technical - New Dacian's Medicine
Hypoxia,
Polycythemia and Cyanosis (3)
Translation Draft
We're here now with cyanosis.
We're here now with cyanosis.
Cyanosis refers to a
bluish coloration of the skin and mucous membranes, resulting
from an increase in the amount of reduced haemoglobin, or
hemoglobin derivatives, in the small vessels in those areas
(where cyanosis is found). It is usually more evident in the
lips, nail beds, ears and malal eminences. The reddish color of
the skin characteristic in polycytemia vera, must be
distinguished from the actual cyanosis discussed here.
Carboxihemoglobin produces a cherry-colored embellisher rather than cyanosis. The degree of cyanosis depends on the skin pigmentation and the thickness of the hair, as well as the level of capillary of the skin. Clinical detection of the presence and degree of cyanosis is accurate, as demonstrated by oxymetric studies. In some cases, central cyanosis can be detected safely when arterial saturation has decreased to 85%, in other cases, in particular, in people with dark skin, cannot be detected until saturation has decreased to 75%.
The increase in the amount of reduced hemoglobin in the skin vessels, which produces cyanosis, can be caused by an increase in the amount of venous blood in the skin, as a result of the dilation of the venuses and the venous end of the capillaries, but also by a reduction in the oxygen saturation of the capillary blood. In general, cyanosis becomes apparent when the average concentration of low capillary haemoglobin exceeds 50 g/L. The important thing in the production of cyanosis is the absolute amount of low hemoglobin rather than the relative.
Thus, in a patient with severe anemia, the relative amount of reduced hemoglobin in the venous blood can be very high in relation to the total amount of hemoglobin. However, since the concentration of the last is much reduced, the absolute amount of reduced haemoglobin may still be low and therefore patients with severe anaemia and marked arterial desaturation do not develop cyanosis.
Conversely, the higher the total haemoglobin content, the greater the tendency towards cyanosis, so patients with marked polycytemia tend to be cyanoticates at higher levels of arterial oxygen saturation than patients with normal haematocrit levels. Local passive congestion, which also causes an increase in the total amount of reduced haemoglobin in the vessels in the area, can cause cyanosis. Cyanosis is also observed when non-functioning haemoglobin, such as methemoglobin and sulfhemoglobin, is present in the blood.
Cyanosis can be classified into two forms, central and peripheral. In the central form, there is an unsaturation of the arterial blood or an abnormal derivative of hemoglobin and both the mucous membranes and the skin are affected. Peripheral cyanosis is due to a slowdown in blood flow in a territory and an abnormally high extraction of oxygen from normal saturated arterial blood. It is the result of vasoconstriction and decreased peripheral blood flow, as happens in exposure to cold, shock, congestive insufficiency and peripheral vascular diseases.
Often, in these situations, the mucosa of the oral or sublingual cavity can be spared. Clinical differentiation between central and peripheral cyanosis is not always simple, and under certain conditions, such as cardiogenic shock with pulmonary edema, both forms can coexist.
From a differential diagnostic point of view, I'll start with central cyanosis. The reduction of arterial saturation in oxygen results from marked reduction in oxygen pressure in the arterial blood. This can be determined by a decrease in oxygen pressure in the inspired air without sufficient compensation by alveolar hyperventilation to maintain alveolar oxygen pressure.
Cyanosis does not occur to a significant degree by an ascent of 2,500 m, but is marked at an ascent of more than 5,000 m. The explanation becomes clear by studying the "S" shape of the oxygen dissociation curve. At 2,500 m, the oxygen pressure in the inspired air is about 120 mmHg, the alveolar pressure is about 80 mmHg and the hemoglobin is almost completely saturated.
However, at 5,000 m, the oxygen pressure in the atmospheric and alveolar air is about 85 and 50 mmHg respectively, and the oxygen dissociation curve shows that the arterial blood is only 75% saturated. This leaves 25% of hemoglobin in reduced form, a quantity that can be associated with cyanosis in the absence of anaemia.
Similarly, an abnormal hemoglobin with low oxygen affinity causes lower oxygen arterial saturation and, consequently, central cyanosis. Severe pulmonary dysfunction, through alveolar hypoventilation or infusion of unventilated or poorly ventilated lung territories, is a common cause of central cyanosis. It can occur acutely, as in extensive pneumonia or pulmonary edema, or in chronic lung diseases (e.g. in emphysema).
In the last situation, polycytemia is generally present and hippocratic fingers may appear. However, in many chronic lung diseases with fibrosis and obliteration of the capillary vascular bed, cyanosis does not occur because there is a relatively small infusion of unventilated areas. Another cause of low-oxygen arterial saturation is the shunt of systemic venous blood in the arterial circulation. Some congenital heart defects are associated with cyanosis.
Since blood flows from a region with higher pressure to a region with lower pressure, for a heart defect to cause a right-left shunt, it should usually be combined with a distal defect obstructive lesion or increased pulmonary vascular resistance. The most common congenital cardiac lesion associated with cyanosis in adults is the combination of ventricular septum defect and pulmonary artery stenosis (Fallot tetralogy).
The more severe the obstruction, the higher the right-left shunt gradient and the resulting cyanosis. Mechanisms of increased pulmonary vascular resistance, which can produce cyanosis in the presence of intra or extracardiac communications without pulmonary stenosis (Eisenmerger syndrome). In patients with arterial canal persistence, pulmonary hypertension and right-left shunt, differentiated cyanosis occurs (i.e. cyanosis occurs in the lower extremities, but not in the upper extremities).
Arteriovenous pulmonary fistulas can be congenital or acquired, solitary or multiple, microscopic or massive. The degree of cyanosis produced by these butts depends on their size and number. They occur with some frequency in hereditary hemorrhagic telangiectasis. Arterial desaturation in oxygen also occurs in patients with cirrhosis, possibly as a consequence of pulmonary arteriovenous fistulas or venous-pulmonary anastomoses.
In patients with right-left cardiac or pulmonary shunts, the presence and severity of cyanosis depends on the size of the shunt in relation to systemic flow, as well as on oxyhemoglobin saturation of venous blood. In patients with central cyanosis due to arterial discharge into oxygen, the severity of cyanosis increases in proportion to physical exertion.
Increased oxygen extraction from the blood, due to the muscles in activity, causes the venous blood returning to the right side of the heart to be more unsaturated than at rest, and the shunt of this blood or its passage through the lungs incapable of normal oxygenation intensifies cyanosis. Also, as long as systemic vascular resistance normally decreases during physical exertion, the right-left shunt is increased by exertion in patients with congenital heart defects and communication between the two parts of the heart.
Secondary polycytemia commonly occurs in patients with arterial desaturation and contributes to cyanosis. Cyanosis can be produced by small amounts of circulating methemoglobin and even smaller amounts of sulfhemoglobin. Although there are no common causes of cyanosis, these abnormal pigments of hemoglobin should be searched by spectroscopy when cyanosis cannot be explained by the dysfunction of the circulatory or respiratory system. In general, digital hippocraticism is not present. Diagnosis of methemoglobinemia should be suspected if, by mixing the patient's blood in the test tube and exposing it to air, it remains chocolate.
Peripheral cyanosis probably has as the most common cause, generalized vasoconstriction, which occurs through exposure to air or cold water, which is a physiological response of the body. When cardiac flow is low, as in congestive heart failure or shock, vasoconstriction of the skin occurs as a compensatory mechanism, so that blood is diverted from the skin stothers to more important territories, such as the central nervous system and the heart, and can result in intense cyanosis associated with cold extremities.
Even if the arterial blood is normally saturated in oxygen, low volume of flow through the skin and low oxygen pressure at the venous end of the capillaries cause cyanosis. Arterial obstruction, e.g. embolic, extremity or arteriolar constriction, as in cold vasospasm (Raynaud phenomenon), generally causes pallor and coldness, but these may also be associated with cyanosis. Although there is a venous obstruction and the extremity is congested, as in the stagnation of blood flow, cyanosis is also present.
Venous hypertension, which may be local (as in thrombophlebitis) or generalized (as in tricuspid valve disease or constrictive pericarditis), dilated subpapillary nerve plexuses and thus intensifies cyanosis.
From the point of view of the patient's approach, certain characteristics are important to determine the actual cause of cyanosis: 1. the history, in particular the duration (cyanosis present from birth is usually due to congenital malformations) and possible exposure to drugs or chemicals that may produce abnormal types of hemoglobin, 2. clinical differentiation of central cyanosis from peripheral cyanosis; objective highlighting, by physical or radiographic examination of diseases of the respiratory or cardiovascular system; massage, mild heating of the cyanotic extremities will produce increased peripheral blood flow and will cause the disappearance of peripheral cyanosis, but not the central one, 3. the presence or absence of digital hippocraticism; this unaccompanied sign of cyanosis occurs frequently in patients with infectious endocarditis and in combination with ulcerative colitis, may occasionally occur in healthy individuals and in some situations may be of an occupational nature, for example, in blacksmiths; mild cyanosis of the lips and cheeks, without digital hippocraticism, is common in patients with mitral stenosis and is likely due to minimal arterial hypoxia resulting from fibrotic changes in the lungs, secondary to long-term congestion combined with reduced cardiac output; the combination of digital cyanosis-hypocratism is common in patients with certain types of congenital heart defects and is occasionally observed in people with lung diseases, such as pulmonary abscess or pulmonary arteriovenous shunts.
On the other hand, peripheral cyanosis or acute development of central cyanosis is not associated with digital hippocraticism, 4. determination of oxygen pressure or oxygen saturation of arterial blood by spectroscopic method and other blood examinations for abnormal types of hemoglobin.
And since we've been talking so much about hippocraticism, we should have some clarification. Selective, globular enlargement of the distal segment of the fingers of the hands and feet, due to the proliferation of connective tissues, especially on the dorsal surface, is called hippocraticism. This growth occurs in the soft tissues of the nail base.
Hippocraticism can be hereditary, idiopathic or acquired and associated with a variety of disorders, including congenital cyanogen heart defects, infectious endocarditis and numerous lung diseases (including primary or metastatic lung cancer, bronchectasis, pulmonary abscess, cystic fibrosis and mesothelioma), as well as with some gastrointestinal diseases (including regional enteritis, chronic ulcerative colitis and cirrhosis of the liver).
In some patients with primary or metastatic lung cancer, mesothelioma, bronchectasis and cirrhosis of the liver, hippocraticism may be associated with hypertrophic osteoarthropathy. In this situation, the new subperiostal bone formation in the distal diaphyses of the long bones of the extremities produces pain and arthritic changes in the shoulders, knees, ankles, wrists and elbows. Diagnosis of hypertrophic osteoarthropathy can be confirmed by X-ray and bone TC. Although the mechanism of digital hippocraticism is unclear, it appears to be secondary to a substance (probably hormonal) that causes the vessels at the fingertips to dilate.
That's how I finished my job today.
Carboxihemoglobin produces a cherry-colored embellisher rather than cyanosis. The degree of cyanosis depends on the skin pigmentation and the thickness of the hair, as well as the level of capillary of the skin. Clinical detection of the presence and degree of cyanosis is accurate, as demonstrated by oxymetric studies. In some cases, central cyanosis can be detected safely when arterial saturation has decreased to 85%, in other cases, in particular, in people with dark skin, cannot be detected until saturation has decreased to 75%.
The increase in the amount of reduced hemoglobin in the skin vessels, which produces cyanosis, can be caused by an increase in the amount of venous blood in the skin, as a result of the dilation of the venuses and the venous end of the capillaries, but also by a reduction in the oxygen saturation of the capillary blood. In general, cyanosis becomes apparent when the average concentration of low capillary haemoglobin exceeds 50 g/L. The important thing in the production of cyanosis is the absolute amount of low hemoglobin rather than the relative.
Thus, in a patient with severe anemia, the relative amount of reduced hemoglobin in the venous blood can be very high in relation to the total amount of hemoglobin. However, since the concentration of the last is much reduced, the absolute amount of reduced haemoglobin may still be low and therefore patients with severe anaemia and marked arterial desaturation do not develop cyanosis.
Conversely, the higher the total haemoglobin content, the greater the tendency towards cyanosis, so patients with marked polycytemia tend to be cyanoticates at higher levels of arterial oxygen saturation than patients with normal haematocrit levels. Local passive congestion, which also causes an increase in the total amount of reduced haemoglobin in the vessels in the area, can cause cyanosis. Cyanosis is also observed when non-functioning haemoglobin, such as methemoglobin and sulfhemoglobin, is present in the blood.
Cyanosis can be classified into two forms, central and peripheral. In the central form, there is an unsaturation of the arterial blood or an abnormal derivative of hemoglobin and both the mucous membranes and the skin are affected. Peripheral cyanosis is due to a slowdown in blood flow in a territory and an abnormally high extraction of oxygen from normal saturated arterial blood. It is the result of vasoconstriction and decreased peripheral blood flow, as happens in exposure to cold, shock, congestive insufficiency and peripheral vascular diseases.
Often, in these situations, the mucosa of the oral or sublingual cavity can be spared. Clinical differentiation between central and peripheral cyanosis is not always simple, and under certain conditions, such as cardiogenic shock with pulmonary edema, both forms can coexist.
From a differential diagnostic point of view, I'll start with central cyanosis. The reduction of arterial saturation in oxygen results from marked reduction in oxygen pressure in the arterial blood. This can be determined by a decrease in oxygen pressure in the inspired air without sufficient compensation by alveolar hyperventilation to maintain alveolar oxygen pressure.
Cyanosis does not occur to a significant degree by an ascent of 2,500 m, but is marked at an ascent of more than 5,000 m. The explanation becomes clear by studying the "S" shape of the oxygen dissociation curve. At 2,500 m, the oxygen pressure in the inspired air is about 120 mmHg, the alveolar pressure is about 80 mmHg and the hemoglobin is almost completely saturated.
However, at 5,000 m, the oxygen pressure in the atmospheric and alveolar air is about 85 and 50 mmHg respectively, and the oxygen dissociation curve shows that the arterial blood is only 75% saturated. This leaves 25% of hemoglobin in reduced form, a quantity that can be associated with cyanosis in the absence of anaemia.
Similarly, an abnormal hemoglobin with low oxygen affinity causes lower oxygen arterial saturation and, consequently, central cyanosis. Severe pulmonary dysfunction, through alveolar hypoventilation or infusion of unventilated or poorly ventilated lung territories, is a common cause of central cyanosis. It can occur acutely, as in extensive pneumonia or pulmonary edema, or in chronic lung diseases (e.g. in emphysema).
In the last situation, polycytemia is generally present and hippocratic fingers may appear. However, in many chronic lung diseases with fibrosis and obliteration of the capillary vascular bed, cyanosis does not occur because there is a relatively small infusion of unventilated areas. Another cause of low-oxygen arterial saturation is the shunt of systemic venous blood in the arterial circulation. Some congenital heart defects are associated with cyanosis.
Since blood flows from a region with higher pressure to a region with lower pressure, for a heart defect to cause a right-left shunt, it should usually be combined with a distal defect obstructive lesion or increased pulmonary vascular resistance. The most common congenital cardiac lesion associated with cyanosis in adults is the combination of ventricular septum defect and pulmonary artery stenosis (Fallot tetralogy).
The more severe the obstruction, the higher the right-left shunt gradient and the resulting cyanosis. Mechanisms of increased pulmonary vascular resistance, which can produce cyanosis in the presence of intra or extracardiac communications without pulmonary stenosis (Eisenmerger syndrome). In patients with arterial canal persistence, pulmonary hypertension and right-left shunt, differentiated cyanosis occurs (i.e. cyanosis occurs in the lower extremities, but not in the upper extremities).
Arteriovenous pulmonary fistulas can be congenital or acquired, solitary or multiple, microscopic or massive. The degree of cyanosis produced by these butts depends on their size and number. They occur with some frequency in hereditary hemorrhagic telangiectasis. Arterial desaturation in oxygen also occurs in patients with cirrhosis, possibly as a consequence of pulmonary arteriovenous fistulas or venous-pulmonary anastomoses.
In patients with right-left cardiac or pulmonary shunts, the presence and severity of cyanosis depends on the size of the shunt in relation to systemic flow, as well as on oxyhemoglobin saturation of venous blood. In patients with central cyanosis due to arterial discharge into oxygen, the severity of cyanosis increases in proportion to physical exertion.
Increased oxygen extraction from the blood, due to the muscles in activity, causes the venous blood returning to the right side of the heart to be more unsaturated than at rest, and the shunt of this blood or its passage through the lungs incapable of normal oxygenation intensifies cyanosis. Also, as long as systemic vascular resistance normally decreases during physical exertion, the right-left shunt is increased by exertion in patients with congenital heart defects and communication between the two parts of the heart.
Secondary polycytemia commonly occurs in patients with arterial desaturation and contributes to cyanosis. Cyanosis can be produced by small amounts of circulating methemoglobin and even smaller amounts of sulfhemoglobin. Although there are no common causes of cyanosis, these abnormal pigments of hemoglobin should be searched by spectroscopy when cyanosis cannot be explained by the dysfunction of the circulatory or respiratory system. In general, digital hippocraticism is not present. Diagnosis of methemoglobinemia should be suspected if, by mixing the patient's blood in the test tube and exposing it to air, it remains chocolate.
Peripheral cyanosis probably has as the most common cause, generalized vasoconstriction, which occurs through exposure to air or cold water, which is a physiological response of the body. When cardiac flow is low, as in congestive heart failure or shock, vasoconstriction of the skin occurs as a compensatory mechanism, so that blood is diverted from the skin stothers to more important territories, such as the central nervous system and the heart, and can result in intense cyanosis associated with cold extremities.
Even if the arterial blood is normally saturated in oxygen, low volume of flow through the skin and low oxygen pressure at the venous end of the capillaries cause cyanosis. Arterial obstruction, e.g. embolic, extremity or arteriolar constriction, as in cold vasospasm (Raynaud phenomenon), generally causes pallor and coldness, but these may also be associated with cyanosis. Although there is a venous obstruction and the extremity is congested, as in the stagnation of blood flow, cyanosis is also present.
Venous hypertension, which may be local (as in thrombophlebitis) or generalized (as in tricuspid valve disease or constrictive pericarditis), dilated subpapillary nerve plexuses and thus intensifies cyanosis.
From the point of view of the patient's approach, certain characteristics are important to determine the actual cause of cyanosis: 1. the history, in particular the duration (cyanosis present from birth is usually due to congenital malformations) and possible exposure to drugs or chemicals that may produce abnormal types of hemoglobin, 2. clinical differentiation of central cyanosis from peripheral cyanosis; objective highlighting, by physical or radiographic examination of diseases of the respiratory or cardiovascular system; massage, mild heating of the cyanotic extremities will produce increased peripheral blood flow and will cause the disappearance of peripheral cyanosis, but not the central one, 3. the presence or absence of digital hippocraticism; this unaccompanied sign of cyanosis occurs frequently in patients with infectious endocarditis and in combination with ulcerative colitis, may occasionally occur in healthy individuals and in some situations may be of an occupational nature, for example, in blacksmiths; mild cyanosis of the lips and cheeks, without digital hippocraticism, is common in patients with mitral stenosis and is likely due to minimal arterial hypoxia resulting from fibrotic changes in the lungs, secondary to long-term congestion combined with reduced cardiac output; the combination of digital cyanosis-hypocratism is common in patients with certain types of congenital heart defects and is occasionally observed in people with lung diseases, such as pulmonary abscess or pulmonary arteriovenous shunts.
On the other hand, peripheral cyanosis or acute development of central cyanosis is not associated with digital hippocraticism, 4. determination of oxygen pressure or oxygen saturation of arterial blood by spectroscopic method and other blood examinations for abnormal types of hemoglobin.
And since we've been talking so much about hippocraticism, we should have some clarification. Selective, globular enlargement of the distal segment of the fingers of the hands and feet, due to the proliferation of connective tissues, especially on the dorsal surface, is called hippocraticism. This growth occurs in the soft tissues of the nail base.
Hippocraticism can be hereditary, idiopathic or acquired and associated with a variety of disorders, including congenital cyanogen heart defects, infectious endocarditis and numerous lung diseases (including primary or metastatic lung cancer, bronchectasis, pulmonary abscess, cystic fibrosis and mesothelioma), as well as with some gastrointestinal diseases (including regional enteritis, chronic ulcerative colitis and cirrhosis of the liver).
In some patients with primary or metastatic lung cancer, mesothelioma, bronchectasis and cirrhosis of the liver, hippocraticism may be associated with hypertrophic osteoarthropathy. In this situation, the new subperiostal bone formation in the distal diaphyses of the long bones of the extremities produces pain and arthritic changes in the shoulders, knees, ankles, wrists and elbows. Diagnosis of hypertrophic osteoarthropathy can be confirmed by X-ray and bone TC. Although the mechanism of digital hippocraticism is unclear, it appears to be secondary to a substance (probably hormonal) that causes the vessels at the fingertips to dilate.
That's how I finished my job today.
Have a good day!
Dorin, Merticaru