is composed of 4 polypeptides subunits 2alpha and 2 beta
2 forms = T (taut) form has low affinity for O2 and R (relaxed) form has high affinity for O2 (300x).
What special bindings properties does hemoglobin exhibit?
Hemoglobin exhibits positive cooperativity and negative allostery
What increases the formation of T form of hemoglobin?
increased Cl-, H+, CO2, 2,3,-BPG, and temperature
Fetal hemoglobin (2 alpha and 2 gamma subunits) difference from adult form?
has lower affinity for 2,3 BPG than adult hemoglobin and thus has higher affinity for O2.
Oxidized form of hemoglobin (ferric Fe3+) that does not bind O2 as readily , but has increased affinity for cyanide.
What the normal form of iron in hemoglobin?
What is the treatment for cyanide poisoning?
To treat cyanide poisoning , use nitrites to oxidize hemoglobin to methemoglobin, which binds cyanide, allowing cytochrome oxidase to function. Use thiosulfate to bind this cyanide, forming thiocyanate, which is renally excreted.
Form of hemoglobin bound to CO in place of O2. Causes decreased in oxygen binding capacity with a left shit in the oxygen hemoglobin dissociation curve. Decreased oxygen unloading in tissues.
Oxygen - Hemoglobin dissociation curve shifts to the right by
increases in CO2, BPG (2,3BPG), Exercise, Acid/Altitude, Temperature C-BEAT
Oxygen - Hemoglobin dissociation curve shifts to right mean?
There is decreased affinity of hemoglobin for O2 (faciliatates unloading of O2 to tissue)
What is the oxygen-dissociation curve for fetus?
Fetal Hb has higher affinity for oxygen than adult Hb, so its dissociation curve is shifted to the left.
What is the pulmonary artery pressure in pulmonary hypertension?
greater than 25mmHg or greater than 35 mmHg during exercise
What histologic changes occurs in pulmonary hypertension?
arteriosclerosis, medial hypertrophy, and intimal fibrosis of pulmonary arteries
What is primary pulmonary hypertension?
Due to an inactivating mutation in the BMPR2 gene (normally functions to inhibit the vascular smooth muscle proliferation); poor prognosis
What is secondary pulmonary hypertension?
due to COPD (destruction of lung parenchyma) ; mitral stenosis (increases resistance causing increased pressure) ; recurrent thromboemoboli (decreased cross-sectional area of pulmonary vascular bed) ; autoimmune disease ( e.g systemic sclerosis ; inflammation which leads to intimal fibrosis which leads to medial hypetrophy) ; left to right shunt ( leads to increased shear stress leading to endothelial injury); sleep apnea or living at high altitude (hypoxic vasoconstriction)
What is the course of severe respiratory distress?
Cyanosis and RVH then death from decompensated cor pulmonale
What is the equation for pulmonary vascular resistance?
PVR = (P pulm artery - P L atrium)/(Cardiac Output) ; Pulm artery = pressure in pulmonary artery and P L atrium = pulmonary wedge pressure
Vessel radius, viscosity , and vessel length relationship with resistance?
a. Acute increase in ventilation , decreased in PO2 and PCO2 b. Chronicaly there is an increase in ventilation c. Increased in erythropoietin increasing hematocrit and hemoglobin (chronic hypoxia) d. Increases in 2,3-BPG (binds to hemoglobin so that hemoglobin releases more O2) f. Cellular chnages include increases in mitochondria g. Increased renal excretion of bicarbonate ( e.g. can augment by use of acetazolamide) to compensate respiratory alkalosis
What is the responese exercisde?
a. Increased CO2 production b. Increased O2 consumption c. Increased ventilation rate to meet O2 demand d. V/Q ratio from apex to base becomes more uniform e. Increased pulmonary blood flow due to increased cardiac output f. decreased pH during strenous exercise secondary to lactic acidosis
What occurs with PaO2 and PaCO2 during exercise?
No changes , but increased in venous CO2 content and decreased in venous O2 content are seen
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