✓ Receptor types in the ANS
1. Adrenergic receptors (adrenoreceptors)
a. a1 Receptors
■ are located on vascular smooth muscle of the skin and splanchnic regions, the gastrointestinal (GI) and bladder sphincters, and the radial muscle of the iris.
■ produce excitation (e.g., contraction or constriction).
■ are equally sensitive to norepinephrine and epinephrine. However, only norepi-
nephrine released from adrenergic neurons is present in high enough concentrations to activate α1
receptors.
■ Mechanism of action: G
q protein, stimulation of phospholipase C and increase in
inositol 1,4,5-triphosphate (IP3
) and intracellular [Ca2+
].
b. a2 Receptors
■ are located on sympathetic postganglionic nerve terminals (autoreceptors), plate-
lets, fat cells, and the walls of the GI tract (heteroreceptors).
■ often produce inhibition (e.g., relaxation or dilation).
■ Mechanism of action: Gi
protein, inhibition of adenylate cyclase and decrease in cyclic
adenosine monophosphate (cAMP).
c. b1 Receptors
■ are located in the sinoatrial (SA) node, atrioventricular (AV) node, and ventricular
muscle of the heart.
■ produce excitation (e.g., increased heart rate, increased conduction velocity,
increased contractility).
■ are sensitive to both norepinephrine and epinephrine, and are more sensitive than the α1 receptors.
■ Mechanism of action: Gs protein, stimulation of adenylate cyclase and increase in cAMP.
d. b2 Receptors
■ are located on vascular smooth muscle of skeletal muscle, bronchial smooth muscle,
and in the walls of the GI tract and bladder.
■ produce relaxation (e.g., dilation of vascular smooth muscle, dilation of bronchioles, relaxation of the bladder wall).
■ are more sensitive to epinephrine than to norepinephrine.
■ are more sensitive to epinephrine than the α1
receptors.
■ Mechanism of action: same as for β1 receptors.
1. Adrenergic receptors (adrenoreceptors)
a. a1 Receptors
■ are located on vascular smooth muscle of the skin and splanchnic regions, the gastrointestinal (GI) and bladder sphincters, and the radial muscle of the iris.
■ produce excitation (e.g., contraction or constriction).
■ are equally sensitive to norepinephrine and epinephrine. However, only norepi-
nephrine released from adrenergic neurons is present in high enough concentrations to activate α1
receptors.
■ Mechanism of action: G
q protein, stimulation of phospholipase C and increase in
inositol 1,4,5-triphosphate (IP3
) and intracellular [Ca2+
].
b. a2 Receptors
■ are located on sympathetic postganglionic nerve terminals (autoreceptors), plate-
lets, fat cells, and the walls of the GI tract (heteroreceptors).
■ often produce inhibition (e.g., relaxation or dilation).
■ Mechanism of action: Gi
protein, inhibition of adenylate cyclase and decrease in cyclic
adenosine monophosphate (cAMP).
c. b1 Receptors
■ are located in the sinoatrial (SA) node, atrioventricular (AV) node, and ventricular
muscle of the heart.
■ produce excitation (e.g., increased heart rate, increased conduction velocity,
increased contractility).
■ are sensitive to both norepinephrine and epinephrine, and are more sensitive than the α1 receptors.
■ Mechanism of action: Gs protein, stimulation of adenylate cyclase and increase in cAMP.
d. b2 Receptors
■ are located on vascular smooth muscle of skeletal muscle, bronchial smooth muscle,
and in the walls of the GI tract and bladder.
■ produce relaxation (e.g., dilation of vascular smooth muscle, dilation of bronchioles, relaxation of the bladder wall).
■ are more sensitive to epinephrine than to norepinephrine.
■ are more sensitive to epinephrine than the α1
receptors.
■ Mechanism of action: same as for β1 receptors.
Cholinergic receptors (cholinoreceptors)
a. Nicotinic receptors
■ are located in the autonomic ganglia (NN) of the sympathetic and parasympathetic
nervous systems, at the neuromuscular junction (NM), and in the adrenal medulla (NN).
The receptors at these locations are similar, but not identical.
■ are activated by ACh or nicotine.
■ produce excitation.
■ are blocked by ganglionic blockers (e.g., hexamethonium) in the autonomic ganglia,
but not at the neuromuscular junction.
■ Mechanism of action: ACh binds to α subunits of the nicotinic ACh receptor. The nicotinic ACh receptors are also ion channels for Na+ and K+
.
b. Muscarinic receptors
■ are located in the heart (M2), smooth muscle (M3), and glands (M3).
■ are inhibitory in the heart (e.g., decreased heart rate, decreased conduction velocity
in AV node).
■ are excitatory in smooth muscle and glands (e.g., increased GI motility, increased secretion).
■ are activated by ACh and muscarine.
■ are blocked by atropine.
■ Mechanism of action:
(1) Heart SA node: Gi protein, inhibition of adenylate cyclase, which leads to opening of K+ channels, slowing of the rate of spontaneous Phase 4 depolarization, and decreased heart rate.
(2) Smooth muscle and glands:
Gq protein, stimulation of phospholipase C, and increase in IP3 and intracellular [Ca2+].
a. Nicotinic receptors
■ are located in the autonomic ganglia (NN) of the sympathetic and parasympathetic
nervous systems, at the neuromuscular junction (NM), and in the adrenal medulla (NN).
The receptors at these locations are similar, but not identical.
■ are activated by ACh or nicotine.
■ produce excitation.
■ are blocked by ganglionic blockers (e.g., hexamethonium) in the autonomic ganglia,
but not at the neuromuscular junction.
■ Mechanism of action: ACh binds to α subunits of the nicotinic ACh receptor. The nicotinic ACh receptors are also ion channels for Na+ and K+
.
b. Muscarinic receptors
■ are located in the heart (M2), smooth muscle (M3), and glands (M3).
■ are inhibitory in the heart (e.g., decreased heart rate, decreased conduction velocity
in AV node).
■ are excitatory in smooth muscle and glands (e.g., increased GI motility, increased secretion).
■ are activated by ACh and muscarine.
■ are blocked by atropine.
■ Mechanism of action:
(1) Heart SA node: Gi protein, inhibition of adenylate cyclase, which leads to opening of K+ channels, slowing of the rate of spontaneous Phase 4 depolarization, and decreased heart rate.
(2) Smooth muscle and glands:
Gq protein, stimulation of phospholipase C, and increase in IP3 and intracellular [Ca2+].
🧠 Autonomic centers—brain stem and hypothalamus
1. Medulla
■ Vasomotor center
■ Respiratory center
■ Swallowing, coughing, and vomiting centers
2. Pons
■ Pneumotaxic center
3. Midbrain
■ Micturition center
4. Hypothalamus
■ Temperature regulation center
■ Thirst and food intake regulatory centers
1. Medulla
■ Vasomotor center
■ Respiratory center
■ Swallowing, coughing, and vomiting centers
2. Pons
■ Pneumotaxic center
3. Midbrain
■ Micturition center
4. Hypothalamus
■ Temperature regulation center
■ Thirst and food intake regulatory centers
A. Electrocardiogram (ECG) :
1. P wave
👉r epresents atrial depolarization.
■ does not include atrial repolarization, which is “buried” in the QRS complex.
2. PR interval
■ is the interval from the beginning of the P wave to the beginning of the Q wave (initial depolarization of the ventricle).
■ depends on conduction velocity through the atrioventricular (AV) node. For example, if AV
nodal conduction decreases (as in heart block), the PR interval increases.
■ is decreased (i.e., increased conduction velocity through AV node) by stimulation of the sympathetic nervous system.
■ is increased (i.e., decreased conduction velocity through AV node) by stimulation of the
parasympathetic nervous system.
3. QRS complex
■ represents depolarization of the ventricles.
4. QT interval
■ is the interval from the beginning of the Q wave to the end of the T wave.
■ represents the entire period of depolarization and repolarization of the ventricles.
5. ST segment
■ is the segment from the end of the S wave to the beginning of the T wave.
■ is isoelectric.
■ represents the period when the ventricles are depolarized.
6. T wave
■ represents ventricular repolarization.
1. P wave
👉r epresents atrial depolarization.
■ does not include atrial repolarization, which is “buried” in the QRS complex.
2. PR interval
■ is the interval from the beginning of the P wave to the beginning of the Q wave (initial depolarization of the ventricle).
■ depends on conduction velocity through the atrioventricular (AV) node. For example, if AV
nodal conduction decreases (as in heart block), the PR interval increases.
■ is decreased (i.e., increased conduction velocity through AV node) by stimulation of the sympathetic nervous system.
■ is increased (i.e., decreased conduction velocity through AV node) by stimulation of the
parasympathetic nervous system.
3. QRS complex
■ represents depolarization of the ventricles.
4. QT interval
■ is the interval from the beginning of the Q wave to the end of the T wave.
■ represents the entire period of depolarization and repolarization of the ventricles.
5. ST segment
■ is the segment from the end of the S wave to the beginning of the T wave.
■ is isoelectric.
■ represents the period when the ventricles are depolarized.
6. T wave
■ represents ventricular repolarization.
#respiratory_physiology_1
1. Tidal volume (Vt)
■ is the volume inspired or expired with each normal breath.
2. Inspiratory reserve volume (IRV)
■ is the volume that can be inspired over and above the tidal volume.
■ is used during exercise.
3. Expiratory reserve volume (ERV)
■ is the volume that can be expired after the expiration of a tidal volume.
4. Residual volume (RV)
■ is the volume that remains in the lungs after a maximal expiration.
■ cannot be measured by spirometry.
5. Dead space
a. Anatomic dead space
■ is the volume of the conducting airways.
■ is normally approximately 150 mL.
b. Physiologic dead space
■ is a functional measurement.
■ is defined as the volume of the lungs that does not participate in gas exchange.
■ is approximately equal to the anatomic dead space in normal lungs.
■ may be greater than the anatomic dead space in lung diseases in which there are
ventilation/perfusion (V/Q) defects
6. Ventilation rate
a. Minute ventilation is expressed as follows:
Minute ventilation V = ×T Breaths min
b. Alveolar ventilation (Va) is expressed as follows:
V V A T = − ( V B D)× reaths min
1. Tidal volume (Vt)
■ is the volume inspired or expired with each normal breath.
2. Inspiratory reserve volume (IRV)
■ is the volume that can be inspired over and above the tidal volume.
■ is used during exercise.
3. Expiratory reserve volume (ERV)
■ is the volume that can be expired after the expiration of a tidal volume.
4. Residual volume (RV)
■ is the volume that remains in the lungs after a maximal expiration.
■ cannot be measured by spirometry.
5. Dead space
a. Anatomic dead space
■ is the volume of the conducting airways.
■ is normally approximately 150 mL.
b. Physiologic dead space
■ is a functional measurement.
■ is defined as the volume of the lungs that does not participate in gas exchange.
■ is approximately equal to the anatomic dead space in normal lungs.
■ may be greater than the anatomic dead space in lung diseases in which there are
ventilation/perfusion (V/Q) defects
6. Ventilation rate
a. Minute ventilation is expressed as follows:
Minute ventilation V = ×T Breaths min
b. Alveolar ventilation (Va) is expressed as follows:
V V A T = − ( V B D)× reaths min
Physiology via @like
Respiratory_physiology_2
B. Lung capacities
1. Inspiratory capacity
■ is the sum of tidal volume and IRV.
2. Functional residual capacity (FRC)
■ is the sum of ERV and RV.
■ is the volume remaining in the lungs after a tidal volume is expired.
■ includes the RV, so it cannot be measured by spirometry.
3. Vital capacity (VC), or forced vital capacity (FVC)
■ is the sum of tidal volume, IRV, and ERV.
■ is the volume of air that can be forcibly expired after a maximal inspiration.
4. Total lung capacity (TLC)
■ is the sum of all four lung volumes.
■ is the volume in the lungs after a maximal inspiration.
■ includes RV, so it cannot be measured by spirometry
B. Lung capacities
1. Inspiratory capacity
■ is the sum of tidal volume and IRV.
2. Functional residual capacity (FRC)
■ is the sum of ERV and RV.
■ is the volume remaining in the lungs after a tidal volume is expired.
■ includes the RV, so it cannot be measured by spirometry.
3. Vital capacity (VC), or forced vital capacity (FVC)
■ is the sum of tidal volume, IRV, and ERV.
■ is the volume of air that can be forcibly expired after a maximal inspiration.
4. Total lung capacity (TLC)
■ is the sum of all four lung volumes.
■ is the volume in the lungs after a maximal inspiration.
■ includes RV, so it cannot be measured by spirometry
Physiology via @like
#Respiratory_physiology_3
Mechanics of Breathing
Muscles of inspiration
1. Diaphragm
■ is the most important muscle for inspiration.
■ When the diaphragm contracts, the abdominal contents are pushed downward, and
the ribs are lifted upward and outward, increasing the volume of the thoracic cavity.
2. External intercostals and accessory muscles
■ are not used for inspiration during normal quiet breathing.
■ are used during exercise and in respiratory distress.
B. Muscles of expiration
■ Expiration is normally passive.
■ Because the lung–chest wall system is elastic, it returns to its resting position after
inspiration.
■ Expiratory muscles are used during exercise or when airway resistance is increased because
of disease (e.g., asthma).
1. Abdominal muscles
■ compress the abdominal cavity, push the diaphragm up, and push air out of the lungs.
2. Internal intercostal muscles
■ pull the ribs downward and inward.
Mechanics of Breathing
Muscles of inspiration
1. Diaphragm
■ is the most important muscle for inspiration.
■ When the diaphragm contracts, the abdominal contents are pushed downward, and
the ribs are lifted upward and outward, increasing the volume of the thoracic cavity.
2. External intercostals and accessory muscles
■ are not used for inspiration during normal quiet breathing.
■ are used during exercise and in respiratory distress.
B. Muscles of expiration
■ Expiration is normally passive.
■ Because the lung–chest wall system is elastic, it returns to its resting position after
inspiration.
■ Expiratory muscles are used during exercise or when airway resistance is increased because
of disease (e.g., asthma).
1. Abdominal muscles
■ compress the abdominal cavity, push the diaphragm up, and push air out of the lungs.
2. Internal intercostal muscles
■ pull the ribs downward and inward.
Forwarded from Clinical medicine
لم نحلُم بأشياءَ عصيّة!
نحنُ أحياءُ وباقون، وللحلم بقيّة ..
نحنُ أحياءُ وباقون، وللحلم بقيّة ..
#Respiratory_physiology_4
. Compliance of the respiratory system
■ is analogous to capacitance in the cardiovascular system.
■ is described by the following equation:
C V = P
where:
C = compliance (mL/mm Hg)
V = volume (mL)
P = pressure (mm Hg)
■ describes the distensibility of the lungs and chest wall.
■ is inversely related to elastance, which depends on the amount of elastic tissue.
■ is inversely related to stiffness.
■ is the slope of the pressure–volume curve.
■ is the change in volume for a given change in pressure. Pressure can refer to the pressure
inside the lungs and airways or to transpulmonary pressure (i.e., the pressure difference
across pulmonary structures).
1. Compliance of the lungs
■ Transmural pressure is alveolar pressure minus intrapleural pressure.
■ When the pressure outside of the lungs (i.e., intrapleural pressure) is negative, the lungs
expand and lung volume increases.
■ When the pressure outside of the lungs is positive, the lungs collapse and lung volume
decreases.
■ Inflation of the lungs (inspiration) follows a different curve than deflation of the lungs
(expiration); this difference is called hysteresis and is due to the need to overcome
surface tension forces when inflating the lungs.
■ In the middle range of pressures, compliance is greatest and the lungs are most
distensible.
■ At high expanding pressures, compliance is lowest, the lungs are least distensible, and
the curve flattens.
. Compliance of the respiratory system
■ is analogous to capacitance in the cardiovascular system.
■ is described by the following equation:
C V = P
where:
C = compliance (mL/mm Hg)
V = volume (mL)
P = pressure (mm Hg)
■ describes the distensibility of the lungs and chest wall.
■ is inversely related to elastance, which depends on the amount of elastic tissue.
■ is inversely related to stiffness.
■ is the slope of the pressure–volume curve.
■ is the change in volume for a given change in pressure. Pressure can refer to the pressure
inside the lungs and airways or to transpulmonary pressure (i.e., the pressure difference
across pulmonary structures).
1. Compliance of the lungs
■ Transmural pressure is alveolar pressure minus intrapleural pressure.
■ When the pressure outside of the lungs (i.e., intrapleural pressure) is negative, the lungs
expand and lung volume increases.
■ When the pressure outside of the lungs is positive, the lungs collapse and lung volume
decreases.
■ Inflation of the lungs (inspiration) follows a different curve than deflation of the lungs
(expiration); this difference is called hysteresis and is due to the need to overcome
surface tension forces when inflating the lungs.
■ In the middle range of pressures, compliance is greatest and the lungs are most
distensible.
■ At high expanding pressures, compliance is lowest, the lungs are least distensible, and
the curve flattens.
Surfactant
■ lines the alveoli.
■ reduces surface tension by disrupting the intermolecular forces between liquid molecules. This reduction in surface tension prevents small alveoli from collapsing and
increases compliance.
■ is synthesized by type II alveolar cells and consists primarily of the phospholipid
dipalmitoylphosphatidylcholine (DPPC).
■ In the fetus, surfactant synthesis is variable. Surfactant may be present as early as gestational week 24 and is almost always present by gestational week 35.
■ Generally, a lecithin:sphingomyelin ratio greater than 2:1 in amniotic fluid reflects
mature levels of surfactant.
■ Neonatal respiratory distress syndrome can occur in premature infants because of the
lack of surfactant. The infant exhibits atelectasis (lungs collapse), difficulty reinflating the lungs (as a result of decreased compliance), and hypoxemia (as a result of
decreased V/Q
■ lines the alveoli.
■ reduces surface tension by disrupting the intermolecular forces between liquid molecules. This reduction in surface tension prevents small alveoli from collapsing and
increases compliance.
■ is synthesized by type II alveolar cells and consists primarily of the phospholipid
dipalmitoylphosphatidylcholine (DPPC).
■ In the fetus, surfactant synthesis is variable. Surfactant may be present as early as gestational week 24 and is almost always present by gestational week 35.
■ Generally, a lecithin:sphingomyelin ratio greater than 2:1 in amniotic fluid reflects
mature levels of surfactant.
■ Neonatal respiratory distress syndrome can occur in premature infants because of the
lack of surfactant. The infant exhibits atelectasis (lungs collapse), difficulty reinflating the lungs (as a result of decreased compliance), and hypoxemia (as a result of
decreased V/Q