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Total blood volume
75.5 mL/kg in men
66.5 mL/kg in women
ejection fraction
SV/EDV
Blood % of body weight
7%
total blood volume
5/6 L
blood volume composition
55% plasma
45% blood cells
Plasma composition
92% water
7% plasma proteins
blood pH
7.4
plasma proteins in blood
Serum albumin
Serum globulin
Fibrinogen
Regulatory proteins
cellular components of blood
Erythrocytes
Leukocytes
Platelets
other things in blood
Products of tissue metabolism
Nutritive organic materials
Electrolytes
Iron
Products of tissue metabolism in blood
BUN- blood,urine,nitrogen
Nutritive organic materials in blood
amino acids, glucose, cholesterol
electrolytes in blood
fe,na,k,ca
composition of RBCs
most numerous, live for 120 days
4-6 million per cubic mm
rbc Buffer blood
via carbonic anhydrase
what is only found in mature rbc
hemoglobin
hematopoiesis
making rbcs from pluripotent stem cells
made in bone marrow
hematopoietic signs of stress
can release immature cells in emergencies, called reticulocytes
only 1% of blood
hematopoiesis steps
mitotic division
maturation
Erythropoietin
hormone that stimulates erythrocyte production, made in kidneys
Erythropoiesis requirements
Iron
Protein
Minerals
Vitamins
intrinsic factor
needed to absorb vitamin B12
Erythropoiesis regulation
by concentration of hemoglobin in blood
Red Cell Destruction
Methemoglobin is removed by mononuclear phagocytic system
Methemoglobin
oxidized iron 3+, normal heme has iron 2+
reduced by Methemoglobin reductase pathway
Porphyrin is reduced
to bilirubin
bilirubin
pigment released by the liver in bile
Too much bilirubin
jaundice
globin is broken down
into iron and recycled
conjugated bilirubin
excreted in bile
urobilinogen
formed by digestion of bilirubin by intestinal bacteria
How much hemoglobin in blood?
15 g of hemoglobin per 100 mL of blood
In pulmonary capillaries, where PO2 of tissues is high
oxygen binds with hemoglobin
In pulmonary capillaries, where PO2 of tissues is low
oxygen is released from hemoglobin
Oxygen saturation
percentage of hemoglobin bound to oxygen
Oxyhemoglobin dissociation curve
The relationship between the partial pressure of oxygen and hemoglobin saturation
PO2 is high
In the lung
oxygen is loaded onto hemoglobin
PO2 is low
In the tissues
oxygen is unloaded from hemoglobin to tissues
Affinity of hemoglobin for oxygen is affected by
Temperature
Acid-base status
2,3-DPG levels
Carbon dioxide levels
Carbon Dioxide Transport
Carbonic anhydrase in the RBC help to form carbonic acid
Hemoglobin + CO2
Carbaminohemoglobin
Hemoglobin + O2
oxyhemoglobin
Carbonic anhydrase
converts of CO2 and water → HCO3− and H+
called chloride shift
reverse happens in lungs
Haldane Effect
As o2 unloads in lungs causes co2 to load up
if decreased amount of oxygen reaching tissues
results in erythropoietin secretion and production of rbcs
Anemia
Deficit of red blood cells
Low oxygen-carrying capacity results in
hypoxia
Relative anemia
total body size goes up but rbc stays level, eg pregnancy
Absolute anemia
actual decrease in numbers of red cells
causes of absolute anemia
Decreased production
Increased destruction
Polycythemia
Excess of red cells
Increases blood viscosity and volume
General Effects of Anemia
Reduction in oxygen-carrying capacity
(Tissue hypoxia)
Compensatory mechanism to restore tissue oxygenation
increased hr/pulse/blood flow
Increase in 2,3-DPG in erythrocytes
decreased oxygen affinity of hemoglobin in tissues
Increase in erythropoietin activity
Mild anemia
Usually no clinical symptoms
Elderly with cardiovascular, pulmonary disease may have symptoms
Mild to moderate anemia
Fatigue, generalized weakness, and loss of stamina, followed by tachycardia and exertional dyspnea
Moderate to severe anemia
Orthostatic/generalized hypotension, vasoconstriction
pallor
transient murmurs
Intermittent claudication (leg cramps)
Tinnitus
Aplastic Anemia
Stem cell disorder,
reduction of hematopoietic tissue,
fatty marrow replacement, and
pancytopenia (low RBC, WBC, and platelets)
pancytopenia
(low RBC, WBC, and platelets)
Aplastic Anemia cause
chemical/radiation damage to bone marrow
Aplastic Anemia symptoms
Insidious onset of symptoms
Thrombocytopenia (prone to bleeding)
Neutropenia (prone to infections)
aplastic anemia diagnosed by
bone marrow biopsy
Disease of the young (15 to 25) or old
aplastic anemia treatment
bone marrow transplant, stop further exposure to toxic causes
aplastic anemia prognosis
fatal unless successful transplant
Anemia of Chronic Renal Failure
Failure of the renal endocrine function impairs erythropoietin production and bone marrow compensation.
Decreased RBC count
Anemia of Chronic Renal Failure treatment
dialysis and administration of erythropoietin
high survival rate with therapy
Pernicious anemia
caused by lack of intrinsic factor leading to vitamin B12 deficiency
megaloblasts
large, immature red blood cells
produced by Disruption in DNA synthesis of blast cells
Low folate levels associated with
neural tube deficits
Clinical manifestations of anemia
Low RBC, WBC, and platelet counts with increased MCV
Peripheral nerve degeneration
Treatment of megaloblastic anemia
determine if vitamin B12, folate, or a combined deficiency is the cause
then treat cause
prognosis of megaloblastic anemia
good prognosis, slow healing of nerve damage
Iron Deficiency Anemia
Most common nutritional deficiency in the world
Insufficient iron for hemoglobin synthesis
Iron Deficiency Anemia symptoms
Pica
Koilonychias (spoon-shaped nails)
Blue sclerae
Iron Deficiency Anemia treatments
oral iron supplements
inherited anemic disorders
Thalassemia
Sickle Cell Anemia
Hereditary Spherocytosis
G6PD Deficiency
Thalassemia
Increased RBC destruction (hemolysis)
Associated with mutant genes
Thalassemia treatment
Blood transfusions
Splenectomy
Chelation therapy
Bone marrow transplantation
Sickle Cell Anemia
a genetic disorder that causes abnormal hemoglobin, resulting in some red blood cells assuming an abnormal sickle shape
Sickle Cell Anemia Treatment
stem cell transplant (no cure)
sickle cell prognosis
if no transplant death
G6PD deficiency
Genetic disorder resulting in RBC membrane destruction
primarily in males
G6PD deficiency treatment
avoiding infection
Polycythemia
Excess RBCs
Increased blood viscosity, hypertension
Polycythemia Vera (Primary Polycythemia)
Neoplastic transformation of bone marrow stem cells
polycythemia vera treatment
phlebotomy, chemoradtherapy
polycythemia vera prognosis
poor unless managed
Secondary Polycythemia
Caused by chronic hypoxemia with resultant increase in erythropoietin
Increased RBC production
Secondary Polycythemia treatment
Identify and manage underlying cause of hypoxemia;
phlebotomy may be used to decrease cardiovascular workload
Relative Polycythemia
Caused by dehydration with spurious increase in RBC production
Elevated hematocrit, hemoglobin, and RBC count
Relative polycythemia treatment
Recognize and manage underlying cause
Fluid administration with management of long-term conditions
Determinants of Systemic Blood Pressure
Pressure differences between the left and right sides of the heart produce systemic movement of blood
Arterial blood pressure is produced by
left ventricular contraction pumping blood into aorta
Cardiac output (CO) =
SV (stroke volume)×HR (heart rate)
Systemic Vascular Resistance (SVR)
afterload
afterload is determined by
Radius of arteries
Degree of vessel compliance
End-diastolic volume
preload
preload
Amount of blood returned to the heart
blood pressure (BP)=
CO(cardiac output) ×SVR(Systemic Vascular Resistance)
Arterial Blood Pressure measured by
Pulse pressure=Systolic − diastolic
systole
Contraction of the heart