Physiology

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يوم الأحد تقيم قناة physiology مسابقة في فسيولوجي القلب cardiovascular عشرين سؤال لمن أراد المشاركه التواصل على الرابط التالي

■ A patient is injected with 500 mg of mannitol. After a 2-hour equilibration period, the concentration of mannitol in plasma is 3.2 mg/100 mL. During the equilibration period, 10% of the injected mannitol is excreted in urine. What is the patient’s ECF volume? Volume = Amount/Concentration (Amount injected-Amount excreted)/ Concentration = (500 mg - 50 mg) / (3.2 mg /100 ml) = 14.1 L

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1. Asthma ■ is an obstructive disease in which expiration is impaired. ■ is characterized by decreased FVC, decreased FEV1, and decreased FEV1/FVC. ■ Air that should have been expired is not, leading to air trapping and increased FRC. 2. COPD ■ is a combination of chronic bronchitis and emphysema. ■ is an obstructive disease with increased lung compliance in which expiration is impaired. ■ is characterized by decreased FVC, decreased FEV1, and decreased FEV1/FVC. ■ Air that should have been expired is not, leading to air trapping, increased FRC, and a barrel-shaped chest. a. “Pink puffers” (primarily emphysema) have mild hypoxemia and, because they maintain alveolar ventilation, normocapnia (normal Pco2). b. “Blue bloaters” (primarily bronchitis) have severe hypoxemia with cyanosis and, because they do not maintain alveolar ventilation, hypercapnia (increased Pco2). They have right ventricular failure and systemic edema. 3. Fibrosis ■ is a restrictive disease with decreased lung compliance in which inspiration is impaired. ■ is characterized by a decrease in all lung volumes. Because FEV1 is decreased less than is FVC, FEV1/FVC is increased (or may be normal).

Breathing cycle—description of pressures and airflow 1. At rest (before inspiration begins) a. Alveolar pressure equals atmospheric pressure. ■ Because lung pressures are expressed relative to atmospheric pressure, alveolar pressure is said to be zero. b. Intrapleural pressure is negative. ■ At FRC, the opposing forces of the lungs trying to collapse and the chest wall trying to expand create a negative pressure in the intrapleural space between them. ■ Intrapleural pressure can be measured by a balloon catheter in the esophagus. c. Lung volume is the FRC. 2. During inspiration a. The inspiratory muscles contract and cause the volume of the thorax to increase. ■ As lung volume increases, alveolar pressure decreases to less than atmospheric pres￾sure (i.e., becomes negative). ■ The pressure gradient between the atmosphere and the alveoli now causes air to flow into the lungs; airflow will continue until the pressure gradient dissipates. b. Intrapleural pressure becomes more negative. ■ Because lung volume increases during inspiration, the elastic recoil strength of the lungs also increases. As a result, intrapleural pressure becomes even more negative than it was at rest. ■ Changes in intrapleural pressure during inspiration are used to measure the dynamic compliance of the lung c. Lung volume increases by one Vt. ■ At the peak of inspiration, lung volume is the FRC plus one Vt. 3. During expiration a. Alveolar pressure becomes greater than atmospheric pressure. ■ The alveolar pressure becomes greater (i.e., becomes positive) because alveolar gas is compressed by the elastic forces of the lung. ■ Thus, alveolar pressure is now higher than atmospheric pressure, the pressure gradi￾ent is reversed, and air flows out of the lungs. b. Intrapleural pressure returns to its resting value during a normal (passive) expiration. ■ However, during a forced expiration, intrapleural pressure actually becomes positive. This positive intrapleural pressure compresses the airways and makes expiration more difficult. ■ In COPD, in which airway resistance is increased, patients learn to expire slowly with “pursed lips” to prevent the airway collapse that may occur with a forced expiration. c. Lung volume returns to FRC

Factors that change airway resistance ■ The major site of airway resistance is the medium-sized bronchi. ■ The smallest airways would seem to offer the highest resistance, but they do not because of their parallel arrangement. a. Contraction or relaxation of bronchial smooth muscle ■ changes airway resistance by altering the radius of the airways. (1) Parasympathetic stimulation, irritants, and the slow-reacting substance of anaphylaxis (asthma) constrict the airways, decrease the radius, and increase the resistance to airflow. (2) Sympathetic stimulation and sympathetic agonists (isoproterenol) dilate the airways via b2 receptors, increase the radius, and decrease the resistance to airflow. b. Lung volume ■ alters airway resistance because of the radial traction exerted on the airways by surrounding lung tissue. (1) High lung volumes are associated with greater traction on airways and decreased airway resistance. Patients with increased airway resistance (e.g., asthma) “learn” to breathe at higher lung volumes to offset the high airway resistance associated with their disease. (2) Low lung volumes are associated with less traction and increased airway resistance, even to the point of airway collapse. c. Viscosity or density of inspired gas ■ changes the resistance to airflow. ■ During a deep-sea dive, both air density and resistance to airflow are increased. ■ Breathing a low-density gas, such as helium, reduces the resistance to airflow.

Surfactant ■ lines the alveoli. ■ reduces surface tension by disrupting the intermolecular forces between liquid mol￾ecules. 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 gesta￾tional 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 reinflat￾ing the lungs (as a result of decreased compliance), and hypoxemia (as a result of decreased V/Q

#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.

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#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.

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

#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

1. Which part of the ECG corresponds to ventricular repolarization? A) the P wave B) the QRS duration C) the T wave D) the U wave E) the PR interval

A. Electrocardiogram (ECG) : 1. P wave ■ 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.

Autonomic nervous system done ✓

🧠 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 centersE. 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

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 nic- otinic 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+].

✓ 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.

👉Organization of the autonomic nervous system. ACh = acetylcholine; CNS = central nervous system.

B. Neurotransmitters of the ANS ■ Adrenergic neurons release norepinephrine as the neurotransmitter. ■ Cholinergic neurons, whether in the sympathetic or parasympathetic nervous system, release acetylcholine (ACh) as the neurotransmitter. ■ Nonadrenergic, noncholinergic neurons include some postganglionic parasympathetic neurons of the gastrointestinal tract, which release substance P, vasoactive intestinal peptide (VIP), or nitric oxide (NO).