A & P 2 - Respiratory 5-6

Front 1

What is the oxygen content in the blood?

Back 1

O2 content in systemic blood at sea level:
-Arterial blood PO2 = 100 mm Hg
-O2 physically dissolved = 3 ml/L
-O2 reversibly bound to Hb = 197 ml/L (totaly = 200 ml/L)
-due to incomplete saturation = 195 ml/L
Venous blood:
-PO2 = 40 mm Hg
-1.2 ml/L dissolved O2
-151 ml/L O2 bound to Hb

amt carried in tissues:
5 L/min (CO) x 200 ml/L = 1000 mlO2/min

Front 2

How is Physically dissolved O2 important?

Back 2

physically dissolved O2 is important because it determines O2 tension in the blood

Front 3

What are the different reactions between O2 and Hb?

Back 3

Oxyhemoglobin:
-binding of oxygen to Hb (loading reaction) does not change ferrous form of iron

Oxidized or methemoglobin:
-cannot transport oxygen because does not have electron to form bond with oxygen
-decreases HbO2 in blood

Deoyxgenated or reduced Hb:
-unloading reaction, dissociation of oxyHb

CarboxyHb:
-Hb + CO
-gas competes with O2 for binding sites on Hb (210x greater than O2 affinity)
-CO decreases oxygenation of blood in pulmonary capillaries and concentration of oxyHb in arterial blood
-shifts to LEFT decreasing dissociation of HbO2 in tissue capillaries

Direction of rxn between O2 and Hb determined by:
O2 tension - high tension favors oxygenation, low tension promotes dissociation
Affinity - high affinity favors loading, low favors unloading

Front 4

What is the Hb saturation in arterial and venous blood?

Back 4

fraction of total Hb in form of oxyHb

% saturation = O2 bound to Hb/O2 carrying capacity X 100, depends ONLY on PO2

arterial blood = 97 % saturation, venous blood = 75 % saturation

percent of oxygen unloaded = 97 - 75 = 22 %

Front 5

What are characteristics of the Oxygen-Hemoglobin Dissociation curve?

Back 5

relates percent of Hb saturation to O2 tension

called association curve

sigmoid shape due to varying affinities of heme groups of O2 (each heme has 4 subunits)

Flat portion (plateau):
-between 70 - 100 mm Hg PO2
-provides adequate saturation of Hb when PO2 in atmospheric or alveolar air reduces (high altitudes, speeach, cardiac diseases etc)

Steep portion:
-between 10 - 70 mm Hg PO2
-works in tissue capillaries, where there is low PO2 and need O2 the most, HbO2 can unload the most

Front 6

What are some factors that affect the dissociation curve?

Back 6

increase PCO2, decrease pH, increase temp, increase DPG --> shifts curve to right (Hb has less affinity for O2 leading to increase dissociation of HbO2)

decrease PCO2, increase pH, decrease temp, decrease DPG --> shift curve to left, Hb has higher affinity for O2

effect of pH:
-increase H+ --> increase binding of H+ to Hb --> decrease affinity for O2 (Bohr effect) --> release of O2 in more active tissues

effect of PCO2:
-increase PCO2 --> decrease pH (Bohr effect) --> carbamino-Hb --> decrease Hb affinity for O2

effect of temp:
-increase temp alters configuration of Hb --> less of affinity of Hb for O2

DPG or BPG:
-produced in RBC by glycolysis
-DPG binds reversibly with HbO2 which releases O2
-production increases in chronic hypoxia, alkalosis, releases O2 from Hb as blood goes from capillaries to tissues

Front 7

What is Myoglobin?

Back 7

present in striated and cardiac muscle cells

1 hem to combine with 1 O2, storage function of O2

higher affinity for O2 than Hb --> myoglobin dissociation curve is to the left of Hb curve

Front 8

How is O2 transfer different in the fetus than mother and what can be a complication?

Back 8

Fetal RBC CANNOT bind to 2,3 DPG

HbF has higher affinity for O2 than adult Hb, curve is to the LEFT of the maternal one

fetal blood takes up O2 from maternal blood and after equilibration is MORE saturated with O2 than maternal blood

unloading of CO2 causes double Bohr effect --> widening gap between two curves causing further shift of O2 towards the fetus

fetal tissue hypoxia:
-increased uptake makes it harder to release O2 to tissues

Front 9

What is the blood CO2 content?

Back 9

Arterial blood:
-PCO2 = 40 mm Hg - 480 ml/L (48 vol %)

Capillaries:
-40 ml/L

Venous blood:
PCO2 = 46 mm Hg - 520 ml/L (480 + 40)

Front 10

What are the forms of CO2 transport?

Back 10

In plasma (70%):
-physically dissolved
-carbamino compound of plasma protein, reversible bind of amino groups of proteins
-bicarbonate = rapidly formed in RBC and diffused in plasma (60%)
-formation of carbonic acid is slow but dissociation of carbonic acid into bicarbonate and H+ is fast

RBC (30%):
-dissolved
-rapidly formed bicarbonate (20%); carbonic anhydrase in RBC increases rate of carbonic acid formation; bicarbonate diffuse down concentration gradient in exchange for Cl- (chloride shift)
-H+ buffered by deoxyHb
-carbamino-Hb, reversible binding to amino groups of Hb

Front 11

What happens in a chloride shift?

Back 11

diffusion of HCO3 along concentration gradient into plasma --> decrease intracellular anions --> diffusion of Cl- into RBCs

this leads to increase osmolarity of ICF and preservation of electrical neutralities which causes increased diffusion of HCO3 into the plasma

Front 12

What happens with CO2 in the pulmonary capillaries?

Back 12

diffuses from blood into alveolar air

CO2 tension decreases --> CO2 released from Hb and formation of oxyHb

binding of O2 to Hb decreases Hb affinity for H+ --> release H+ from Hb

H+ combines with bicarbonate to make carbonic acid

when CO2 tension in blood decreases carbonic anhydrase catalyzes conversion of carbonic acid to CO2 and water

REVERSE CHLORIDE SHIFT

Front 13

What is characteristic of the CO2 dissociation curve?

Back 13

pretty much linear

influenced by degree of oxygenation of the blood - Haldane effect:
-HbO2 has weaker affinity for CO2 than deoxy-Hb --> shifts curve to right
-Deoxy-Hb is a better buffer than oxy-Hb --> decreases concentration of H+ shifts reaction CO2 + H20 --> HCO3 + H+ to the right (makes it faster)

Front 14

What is the Respiratory Quotient?

Back 14

RQ = Volume CO2 produced / Volume O2 consumed

Carbs = 1
Fats = 0.7
Proteins = 0.8
Mixed diet = 0.8

Front 15

What are the respiratory neurons involved in neural regulation of respiration?

Back 15

LMN:
-cervical --> phrenic --> diaphragm
-thoraci --> intercostals --> intercostal mm
DIRECT innervation

UMN:
-medulla, pons, higher centers (cerebral cortex, hypothalamus, limbic system, cerebellum)
-responsible for breaking pattern and respiratory rhythm
-breathing pattern is from medulla

Front 16

What are the brain stem respiratory centers?

Back 16

Rhythmicity area:
Dorsal Respiratory Group (DRG):
-pacemaker

Front 17

What are the centers in the Pontine Respiratory group?

Back 17

Pneumotaxic center:
-activated by impulses from inspiratory neurons
-inhibitory effect on inspiration (same function as vagus), inhibits apneustic center and prevention of apneusis
-volume limiting and rate controlling --> increase rate of respiration

Apneustic center:
-controls depth of inspiration
-causes apneusis - long and powerful inspiration and brief expiration

Front 18

What are the effects of other brain centers on respiration?

Back 18

Reticular Activating System (RAS):
-stimulates ventilation
-impt drive in people with drug overdose

Higher brain centers:
Hypothalamus:
-continual background excitatory drive to DRG and stimulation of breathing during fever etc
Limbic system:
-emotion
Cerebellum:
-respiration in exercise

Voluntary control of respiration:
-voluntary control bypasses respiratory centers and travels in pyramidal system directly to LMN

Front 19

What are the reflexes of respiration?

Back 19

Hering-Breuer inflation reflex:
-stretching of airway and visceral pleura during lung inflation --> 'Off switch' terminates inspiration causing bronchodilation and increase HR by CN X

Distension and distortion of the pulmonary microvasculature:
-increase in interstitial fluid (edema, emboli) + substances released (histamine) --> activation of J receptors (juxtacapillary) --> dsypnea, rapid shallow breathing

Feedback control of contraction of respiratory mm and position of chest wall:
-afferent impulses contain information about length of mm. and position of chest wall, activation causes dyspnea

Protective reflexes:
-irritant receptors activate coughing and sneezing

Front 20

What are the chemical controls of respiration?

Back 20

Central chemoreceptors:
-located in chemosensitive area of medulla
-indirectly monitor blood PCO2 by changes in PO2, pH and brain ECF
-BBB is highly permeable to CO2 and O2 but not H+, CO2 then reacts with water for form carbonic acid
-H+ in brain ECF is PRIMARY stimulus for chemoreceptors, CO2 has very little direct put potent INDIRECT effect
-react more slowly to hypercapnia but responsible for 80 % of the response to increased bicarbonate in blood

Peripheral:
-located in aortic and carotid bodies
-sensitive to decrease PO2 in arterial blood
-stimulated by hypercapnia associated with increase in H+ ions in blood (acidity)

Front 21

What is the importance of peripheral chemoreceptors?

Back 21

responds to excess CO2 more rapidly than central and can maintain response longer

reacts DIRECTLY with increased arterial H+

only place that monitors O2 blood level

initiates non-respiratory responses:
-increase HR
-constriction of peripheral blood vessels
-increase activity of adrenal glands

Front 22

What are physiological changes of respiration during exercise?

Back 22

1. increase minute ventilation

2. increase O2 uptake by pulmonary blood:
-due to increase opening of capillaries --> increase SA of alveolar-capillary membrane
-increase rate of blood flow
-increase diffusion capacity for O2

3. Increase in O2 uptake by tissues:
-increase metabolic rate in skeletal muscles --> decrease PO2 in tissues
-increase alveolar-venous blood PO2 gradient

4. Increase CO2 output

5. Increase energy requirement for respiratory muscle contraction

Front 23

What are the controls of respiration in exercise?

Back 23

light exercise:
-PO2, PCO2, and pH remain constant, cannot affect chemoreceptors to change breathing pattern

Severe exercise:
-accumulation of lactic acid (metabolic acidosis) --> hyperpnea

Neural mechanisms:
-collateral impulses from brain motor areas
-body proprioceptors
-conditioned reflexes (increase in ventilation before exercise begins)

Humoral mechanisms:
-increase Adr and NAdr
-increase fluctuations in arterial PCO2 during respiratory cycle
-increase body temp

Front 24

What is Hypoxia and the various types?

Back 24

decrease in PO2 in peripheral tissues

anoxia - extreme hypoxia

effects:
-brain is most sensitive

Types:
Hypoxic:
-arterial PO2 below normal range (hypoxemia)
Anaemic:
-decrease RBC, decrease Hb, metHb; arterial PO2 is normal but O2 is lower
Ischemic (stagnant, hypokinetic):
-reduced blood flow and decreased O2 delivery to tissues
Histotoxic:
-results from action of toxic agents (cyanide poisoning); arterial PO2 is normal but cells cannot utilize O2 properly

Front 25

What are the effects of Low atmospheric response?

Back 25

example is high altitude

Acute:
-hyperventilation --> activation of peripheral chemoreceptors --> lower arterial PCO2 --> hypocapnia and respiratory alkalosis --> decrease respiratory drive at central chemoreceptors level
-Tachycardia
-decrease mental proficiency --> decrease performance of discrete motor movements
-cyanosis

Chronic:
-increase pulmonary diffusing capacity
-increase capillarity in tissues --> increase O2 transfer and utilization in mitochondria
-increased myoglobin content of skeletal mm
-increase in DPG production
-increase in EPO secretion