Ursharona's List: physiology

• each gas has a partial pressure which is the pressure which the gas would have if it alone occupied the volume.^[
• total pressure of a gas mixture is the sum of the partial pressures of each individual gas in the mixture.
• is a measure of thermodynamic activity of the gas's molecules
• Gases will always flow from a region of higher partial pressure to one of lower pressure; the larger this difference, the faster the flow.
• Gases dissolve, diffuse, and react according to their partial pressures, and not according to their concentrations in gas mixtures or liquids.

• The partial pressures of particularly oxygen (PO₂) and carbon dioxide (PCO₂) are important parameters in tests of arterial blood gases, but can also be measured in, for example, cerebrospinal fluid.

                                     

  Reference ranges for PO₂ and PCO₂

  	Unit	Arterial blood gas	Venous blood gas	Cerebrospinal fluid	Alveolar pulmonary  gas pressures
  PO2	kPa	11–13[10]	4.0–5.3[10]	5.3–5.9[10]	14.2
  	mmHg	75–100[11]	30–40[12]	40–44[13]	107
  PCO2	kPa	4.7–6.0[10]	5.5–6.8[10]	5.9–6.7[10]	4.8
  	mmHg	35–45[11]	41–51[12]	44–50[13]	36

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• easy way to think of partial pressure in scuba diving is to consider it a measurement of the concentration of a particular gas
• extremely high partial pressures of oxygen may be toxic (oxygen toxicity) and very high concentrations of some gases, such as nitrogen, may cause narcosis.
• Two factors determine the partial pressure of a gas in scuba diving – the percentage (or fraction) of the gas in the breathing mixture and the depth (and therefore the ambient pressure) at which a diver breathes the gas.
• The higher the percentage of a gas and the deeper a diver descends, the greater the partial pressure of the gas.

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• Airway obstruction is a respiratory problem caused by increased resistance in the bronchioles (usually from a decreased radius of the bronchioles)
• It is different from airway restriction (which prevents air from diffusing into the pulmonary arteries because of some kind of blockage in the lungs).
• A decreased FEV1/FVC ratio (versus the normal of about 80%) is indicative of an airway obstruction,
• as the normal amount of air can no longer be exhaled in the first second of expiration
• An airway restriction would not produce a reduced FEV1/FVC ratio, would produce a reduced vital capacity
• The ventilation is therefore affected leading to a ventilation perfusion mismatch and hypoxia.

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• Cardiac tamponade is compression of the heart that occurs when blood or fluid builds up in the space between the myocardium (heart muscle) and the pericardium (outer covering sac of the heart).

  Causes, incidence, and risk factors

  In this condition, blood or fluid collects in the pericardium. This prevents the ventricles from expanding fully. The excess pressure from the fluid prevents the heart from functioning normally.

• ngina pectoris–commonly known as angina–is chest pain due to ischemia of the heart muscle, generally due to obstruction or spasm of the coronary arteries
• Angina pectoris,
• main cause of Angina pectoris is Coronary Artery Disease, due to atherosclerosis of the arteries feeding the heart.
• derives from the Latin angina ("infection of the throat") from the Greek ἀγχόνη ankhonē ("strangling"), and the Latin pectus ("chest"), and can therefore be translated as "a strangling feeling in the chest".
• chest pain^[1] due to ischemia (a lack of blood, thus a lack of oxygen supply and waste removal) of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels)
• is due to atherosclerosis of the cardiac arteries
• likelihood

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• Afterload can be thought of as the "load" that the heart must eject blood against
• closely related to the aortic pressure.
• related to ventricular wall stress (σ)
• wall stress is wall  tension divided by wall thickness
• wall tension (T) is proportionate to the pressure (P) times  radius (r) for thin-walled spheres or cylinders.
• . A hypertrophied ventricle (thickened wall) reduces wall stress and afterload.
• Hypertrophy  can be thought of as a mechanism that permits more muscle fibers (actually, sarcomere units) to share in the wall tension that is  determined at a give pressure and radius
• The thicker the wall, the less tension  experienced by each sarcomere unit.
• Briefly, an increase in afterload decreases the velocity of fiber shortening
• Afterload is increased when aortic pressure and systemic vascular resistance are increased, by aortic valve stenosis, and by ventricular dilation.
• The interaction between afterload and preload is utilized in the treatment of heart failure,  in which vasodilator drugs are used to augment stroke volume by decreasing afterload, and at the same time, reduce ventricular preload
• When arterial  pressure is reduced, the ventricle can eject blood more rapidly, which increases  the stroke volume and thereby decreases the end-systolic volume.
• Stroke volume increases overall because the  reduction in end-diastolic volume is less than the reduction in end-systolic  volume.

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• Voltage-gated sodium channels have three types of states: deactivated (closed), activated (open), and inactivated (closed)
• The ability to inactivate is thought to be due to a tethered plug (formed by domains III and IV of the alpha subunit), called an inactivation gate, that blocks the inside of the channel shortly after it has been activated. During an action potential the channel remains inactivated for a few milliseconds after depolarization. The inactivation is removed when the membrane potential of the cell repolarizes following the falling phase of the action potential. This allows the channels to be activated again during the next action potential.
• Genetic diseases that alter sodium channel inactivation can cause muscle stiffness or epileptic seizures because of the introduction of a so-called window current, during which sodium channels are tonically active, causing muscle and/or nerve cells to become over-excited.

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• Deoxygenation of the blood increases its ability to carry carbon dioxide;
• Carbon dioxide can bind to amino groups, creating carbamino compounds. Amino groups are available for binding at the N-terminals and at side-chains of arginine and lysine residues in hemoglobin. This forms carbaminohemoglobin.
• Carbaminohemoglobin is the major contributor to the Haldane effec
• Histidine residues in hemoglobin can accept protons and act as buffers. Reduced (deoxygenated) hemoglobin is a better proton acceptor than the oxygenated form.^[
• In red blood cells, the enzyme carbonic anhydrase catalyzes the conversion of dissolved carbon dioxide to carbonic acid, which rapidly dissociates to bicarbonate and a free proton:
   CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃^-
   By Le Chatelier's principle, anything that stabilizes the proton produced will cause the reaction to shift to the right, thus the enhanced affinity of deoxyhemoglobin for protons enhances synthesis of bicarbonate and accordingly increases capacity of deoxygenated blood for carbon dioxide.
• In patients with lung disease, lungs may not be able to increase alveolar ventilation in the face of increased amounts of dissolved CO₂.

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• It acts mainly on the distal tubules and collecting ducts of the nephron, the functional unit of the kidney, to cause the conservation of sodium, secretion of potassium, increased water retention, and increased blood pressure.
• Its activity is reduced in Addison's disease and increased in Conn's syndrome.

• Cardiac syndrome X is angina (chest pain)
• decreased blood flow to heart tissue but with normal coronary arteries
• It is treated with calcium channel blockers,
• It is believed that the lack of blood flow caused by a microvascular disease and the enhanced pain perception are two of the factors that may cause it.
• narrowing of these vessels may lead to the lack of oxygen in specific areas of the cardiac muscle which causes chest pain.
• atients suffering from Syndrome X have enhanced pain perception and they usually feel more intense chest pain than the individuals without Syndrome X
• risk factors include abdominal obesity, meaning the excessive fat tissue in and around the abdomen, atherogenic dyslipidemia which is a blood fat disorder, and elevated blood pressure.^[2] Other risk factors are the insulin resistance or intolerance to glucose, prothrombotic state or proinflammatory state.

• In a large percentage of patients, there is a finding of systemic microvascular abnormalities, causing reduced blood flow in the microvasculature of the cardiac muscles.

   

  While numerous physiological mechanisms have been proposed, none have been proven.

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• physiological nervous system response to increased intracranial pressure (ICP) that results in Cushing's triad of widening pulse pressure, irregular breathing, and a reduction of the heart rate
• seen in the terminal stages of acute head injury and may indicate imminent brain herniation. It can also be seen after the intravenous administration of epinephrine and similar drugs.^[
• classically presents as an increase in systolic and pulse pressure, reduction of the heart rate (bradycardia), and irregular respiration.
• caused by increased pressure inside the skull.^[4] These symptoms can be indicative of insufficient blood flow to the brain (ischemia) as well as compression of arterioles.^[
• In response to rising intracranial pressure (ICP), respiratory rate increases.^[6] The increase in ventilation is exhibited as an increase in rate rather than depth of ventilation, so the Cushing reflex is often associated with slow, irregular breathing.

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• Individuals with WPW have an accessory pathway that communicates between the atria and the ventricles, in addition to the AV node. This accessory pathway is known as the bundle of Ken
• This accessory pathway does not share the rate-slowing properties of the AV node, and may conduct electrical activity at a significantly higher rate than the AV node.