Anästhesie (Fach) / Physiologie (Lektion)
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- Breathing systems The Conway classification includes four categories Open Semi-open, for example, Schimmelbusch mask Semi-closed, for example, the Mapleson classification Closed, for example, the circle. Mapleson classified breathing systems into five groups A to E: Mapleson A, for example, Magill and Lack (coaxial A) Mapleson B Mapleson C Mapleson D, for example, Bain (coaxial D) Mapleson E (T piece). Jackson Rees later modified the Mapleson E by adding an open ended bag, which has since become known as the Mapleson F. Mapleson A/ Magill- efficient for spontaneous breathing requiring gas flow at the patient's alveolar volume (70 ml/kg/min). Ab 25 kg. The Magill and the Lack (a coaxial system) are both classified as Mapleson A systems and they are inefficient during controlled ventilation. Lack system or coaxial Mapleson A, where the fresh gas flows through an outer tube (30 mm) and exhaled gases flow through the inner tube (14 mm). very efficient for spontaneous breathing (more than any other of the Mapleson circuits). Mapleson B and C - inefficient for both SV and PPV; requires gas flow of two to three times minute volume (100 ml/kg/min) Mapleson D (Beutel mit T-Stück, Reservoir und Ventil)- Frischgaszufuhr: 150-250 ml/kg/min (spontanatmung), 70 ml/kg/min (IPPV).The Bain circuit is a "coaxial" Mapleson D - the same components, but the fresh gas flow tubing is directed within the inspiratory limb, with fresh gas entering the circuit near the mask. Fresh gas flow requirements are similar to other NRB circuits. They are very inefficient during spontaneous ventilation. The Bain has been shown to add more heat and humidity to inhaled gases than other Mapleson circuits. Mapleson E and F - for paediatric use; requires gas flow at two to three times the patient's minute volume. The Mapleson F consists of an open-ended reservoir bag (Jackson-Rees modification). The Humphrey ADE system may change the characteristics of the circuit into a Mapleson A, D or E dependent on the position of a lever. The Manley ventilator is a minute volume divider and has two bellows and three valves. The total flow set at the flowmeters is the minute volume; therefore the Manley is classed as a minute volume divider. The tidal volume is preset. It does have the appropriate connections compatible with anaesthetic gas scavenging systems. In spontaneous ventilation it acts as a Mapleson D breathing system (not Mapleson E), which requires high fresh gas flows to prevent rebreathing.
- oxygen cascade is a series of steps where the PO2 falls from atmospheric air to the intracellular mitochondria The greatest drop in PO2 is between the artery (13.3 kPa or 100 mmHg) and the mitochondria (1-5 kPa or 7.5-40 mmHg). The PO2 does drop by about one third between the air (21 kPa or 160 mmHg) and alveolus (14 kPa or 106 mmHg). Humidified tracheal gas has a PO2 of 19.8 kPa (150 mmHg) and capillaries has a PO2 of 6-7 kPa (45-55 mmHg). The alveolar PCO2 is normally between 4.7-6.0 kPa (35-45 mmHg) .
- Respiratorische Kontrolle durch: carotid bodies. Pulmonary stretch receptors (in airway smooth muscle): respond to distension of the lung. Juxta capillary receptors (in alveolar walls) painful stimulus: may lead to apnoea and can be followed by a period of hyperventilation. aortic and carotid sinus baroreceptors: stimulated by an increase in the blood pressure -> Reflex apnoea or hypoventilation
- pulmonal arterielle Hypertonie > 30/15 mmHg bzw. mittlerer Druck > 20 mmHg causes: elevate capillary and pulmonary venous pressure; decrease the arterial cross-sectional area; or increase pulmonary artery blood flow. Crotalaria Vergiftung, Appetitzügler, orale Kontrazeptiva > reducing the arterial cross-sectional area Eisenmenger's syndrome: occurs when patients (with septal defects or PDA) develop irreversibly increased pulmonary arterial pressure, causing the left to right shunt to convert to a right to left shunt
- Schrittmacherzellen Herz Pacemaker cell action potentials are made up of phase 4 (spontaneous slow diastolic depolarisation by ‘funny’ currents and calcium influx through T-type channels), phase 0 (depolarisation by calcium influx through L-type channels) and phase 3 (repolarisation by potassium efflux). Parasympathetic stimulation causes hyperpolarisation of the cell through increased potassium permeability whereas sympathetic stimulation increases excitability by opening calcium channels. Phase 0 (depolarisation) in pacemaker cardiac cells differs from that in non-pacemaker cells and muscle and nerve cells - it is primarily mediated by inward calcium influx rather than sodium influx as in the other cell types. Phase 4 is indeed the spontaneous depolarisation from maximum diastolic potential of −45 to −55 mV, to the threshold potential of approximately −40 mV. The depolarisation of cardiac pacemaker and non-pacemaker cells lasts for approximately 200-400 milliseconds, as distinct from the much shorter nerve action potentials lasting approximately 1 millisecond. The depolarisation plateau (phase 2) involves the opening slow calcium channels in non-pacemaker cardiac cells. However, there is no plateau phase in the SA node action potential, which consists of phases 4, 0 and 3 only.
- Cerebraler Blutfluss Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) − intracranial pressure (ICP). Typical values are: MAP = 90 mmHg and ICP = 12. Normal CPP ranges between 75-85 mmHg. Cerebral blood flow (CBF) is approximately 50ml/100g of brain tissue per minute and is maintained at this constant rate over a wide range of mean arterial pressures (not systolic blood pressures). This phenomenon is called autoregulation and occurs between mean arterial pressures (MAP) of 60 - 160 mmHg in a normotensive patient. This range can vary according to source information. The range is sometimes quoted in terms of systolic blood pressure of 80 - 180mmHg The autoregulation curve for cerebral blood flow is shifted to the right (not left) with hypertension and is lost around areas of diseased brains. CBF increased by Hypercapnia, cerebral vasodilatation linear relationship between PaCO2 and CBF from around 3.5-10.0 kPa. At 10kPa CBF is around 120 ml/100g. PaO2 below 6.7kPa (50 mmHg), doubled at a PaO2 of 4 kPa (30 mmHg) General anaesthesia (vasodilation) Hypoxia Lower plasma viscosity Ketamin (increases cerebral metabolic rate and hence blood flow) CBF reduced by (hyperoxia) hypocapnia, cerebral vasoconstriction (reduction in PaCO2 from 5 kPa to 4 kPa (40 to 30 mmHg) results in a 30% fall in blood flow) Hypothermia (temperature below 35°C)
- Schwangerschaft, Veränderungen Abnahme Bicarbonat (18-20 mmol/L; Kompensation der respiratorischen Alkalose) Plasmacholinesterase FRC (um 20%) TotalLungCapacity (um 5%) Totale Compliance (Abnahme chest wall compliance bei konstanter Lungencompliance) Systolischer und diastol. RR (um 10% in 20.SSW) Thrombozyten (<5%, Verbrauch > gesteigerte Bildung) tubuläre Reabsorption von Glukose (intermitt. Glucosurie) Wachstumshormon Zunahme Basal metabolic rate, oxygen consumption (um 20%) Tidalvolumen (um 30%) anatomischer Totraum (um 45%) Cardiac output (um bis zu 50%) Stroke volume (um 35%. Linksventrikuläre Hypertrophie) oestrogen, progesteron (Vasodilatation, Zunahme der Herzfrequenz um 15-25%) Aldosteron (Gegensteuerung der natriuretischen Wirkung von Progesteron) Atemfrequenz (Progesteron) PaO2 (bis 14kPa. Am Termin <13,5 wegen erhöhtem O2-Verbrauch) Blutvolumen (um 48%. Erythrozyten und Plasma) Renal erythropoietin increases red cell mass by 20-30% CRP, Blutsenkungsgeschwindigkeit (Hyperfibrinogenämie) Faktoren VII, VIII, IX, X, Fibrinogen. GFR (um 50%) Prolactin, ACTH, Cortisol, Aldosteron, Renin Angiotensin Proteine im Urin (in 20% der normalen SS) NO Produktion Unverändert freies Thyroxin (mehr Thyroxin, aber auch mehr Thyroid bindendes Globulin) ZVD, PCWP 1. The cardiovascular system An increased cardiac output A 30% increase in stroke volume A 15% increase in heart rate Decreased peripheral vascular resistance and lowered diastolic blood pressure Increased organ blood flow. 2. The respiratory system An increased minute volume due to a 40% increase in tidal volume (small change in respiratory rate) Decrease in functional residual capacity A respiratory alkalosis An increase in CO2 production. 3. The renal system Increased total body water by up to 8 litres Increased renal plasma flow A 50% increase in glomerular filtration rate (not 25%) A decrease in plasma osmolality (by 10 mosmol/kg) and specific gravity Decreased plasma sodium, potassium, urea and creatinine concentrations Sodium and potassium retention A reduced tubular threshold for glucose. 4. The gastrointestinal system Decreased lower oesophageal sphincter tone. EKG: left axis deviation, depressed ST segments and inversion or flattening of the T-wave in lead III. Post partum Arterial blood gas parameters return to normal after a few days. Blood volume takes eight weeks to return to normal. Cardiac output, stroke volume and heart rate take six to eight weeks post-partum to return to normal levels. Gastric emptying remains reduced for a few days post-partum therefore the increased risk of aspiration should be considered. The white cell count returns to normal after six weeks.
- Opioidrezeptoren They are G-protein coupled receptors (not ligand gated ion channels) and five types have been identified: Mu Delta Kappa Sigma Epsilon.
- Nierenversagen Pre-renal causes of acute renal failure (ARF) are associated with the following urinary findings: Low urinary sodium and chloride concentration (<20 mEq/l) High urinary urea and creatinine concentration (>20 mEq/l) High urine osmolality (>400 mosmol/kg) High urine:plasma osmolality ratio (>1.8). Intrinsic causes of acute renal failure (ARF) for example, acute tubular necrosis are associated with the following urinary findings: High urinary sodium and chloride concentration (>40 mEq/l) Low urinary urea and creatinine concentrations Low urine osmolality (<350) Low urine:plasma osmolality ratio (1.2). It is important to note that the findings listed above may change when pre-renal causes of ARF become superimposed on chronic intrinsic renal failure or following diuretic therapy. The presence of red cell casts suggests acute glomerular damage. Epithelial casts occur in acute tubular damage and forms of acute glomerulonephritis. White cell casts appear in pyelonephritis. Granular casts may indicate tubular damage, but they can also be found in the urine of normal individuals. Hyaline casts may be found during any febrile illness and after loop diuretic therapy.
- Second massanger When an agonist interacts with a receptor on the cell surface, second messengers relay signals to target molecules in the cytoplasm or nucleus. They also amplify the strength of the signal. Calcium is the most ubiquitous and abundant second messenger that regulates multiple cellular functions in the body. These include: Muscle contraction (skeletal, smooth and cardiac) Exocytosis (neurotransmitter release at synapses and insulin secretion) Apoptosis Cell adhesion to the extracellular matrix Activation of lymphocytes Biochemical changes mediated by protein kinase C. cAMP is either inhibited or stimulated by G proteins. The receptors in the body that G stimulating (Gs) increase cAMP include: Beta (β1, β2, and β3) Dopamine (D1 and D5) Histamine (H2) Glucagon Vasopressin (V2). cGMP is the second messenger for the action of nitric oxide (NO) and atrial natriuretic peptide (ANP). IP3 and DAG are the second messengers for angiotensin and thyroid stimulating hormone.
- Muskelkontraktion The normal resting membrane potential is -70 mV. Motor neurone stimulation depolarises the sarcolemma via the end-plate (the action potential lasting 2 - 4 ms), and calcium ions are released from the sarcoplasmic reticulum (SR). Discharge of motoneurones results in the inward spread of depolarisation along T-tubules. Depolarisation of the T-tubule activates the sarcoplasmic reticulum via dihydropyridine receptors, which are voltage-gated Ca2+ channels in the T-tubule membrane. Ca2+ diffuses to thick and thin filaments and binds to troponin C, which displaces tropomyosin and uncovers myosin-binding sites on actin. Hydrolysis of ATP results in cross-linkages between actin and myosin and sliding of thick on thin filaments, producing shortening. This is an active process as Ca2+ is pumped back into the sarcoplasmic reticulum. Muscle relaxation occurs by the re-uptake of calcium ions by the SR and is an active process.
- Augeninnendruck norm: 16 +/- 5 mm Hg. determined by The equilibrium between the production and drainage of aqueous humour Intraocular blood volume (which is affected by central venous pressure) and Scleral rigidity and capacity Abnahme durch: Thiopental, Etomidate Zunahme: MCP, Ketamin
- Bronchialmuskulatur Dilatation: VIP (vasoactive intestinal Peptide), Epinephrine Konstriktion: Schwefeldioxid, Leukotriene, ACh
- thermoregulation Neonates have a large surface area in relation to body mass, low heat production and low tissue insulation all of which predispose to rapid heat loss. They are unable to shiver and produce heat by non-shivering thermogenesis, which involves the oxidation of triglycerides located in brown fat. Brown fat is located at the base of the neck, axillae, inter scapular region and in the mediastinum. An uncovered head can account for 60% of total heat loss. Temperature receptors are located in the skin, CNS and gastrointestinal system and they are more sensitive to rapid changes than to gradual ones. In both neonates and adults the anterior hypothalamus responds to heat and the posterior hypothalamus responds to cold.
- Stress/ chirurgischer Reiz Secretion of anterior pituitary hormones (excluding TSH and the sex hormones) Stimulation of the adrenal gland with secretion of catecholamines and the gluco-and mineralocorticoids and Secretion of glucagon and inhibition of insulin secretion. The principal immunological/inflammatory changes include: Cytokine release (IL 1-17, interferons and TNF). One of the most important markers of tissue damage is IL-6. Acute phase response.
- Anionenlücke Differenzierung zwischen metabolischer Azidose wegen zu wenig Bicarbonat bzw. wegen Zufuhr von Säuren Cl-und Bicarbonat: 85 % der Anionen im Serum Anionenrest (Proteinat, Sulfat, Phosphat, organische Anionen)=Anionenlücke. Berechnung: [K+] + [Na+] - [Cl-] l- [HCO3-] (mmol/l). Normbereich: 12 ± 4 mmol/l Reduziert bei Abnahme des Albumins; Zunahme bei Hyperphosphatämie. The anion gap is likely to be abnormally high in most conditions of acidosis except: Renal tubular acidosis Treatment with acetazolamide and Ureteric implantation into the colon. Erhöhte Anionenlücke bei Methanol Uraemia Paraldehyde Infection Lactic acidosis Ethylene glycol/ethanol Salicylates. Ketoacidose (diabetes, alcohol, starvation) Inability to excrete acids (sulfate and phosphate) secondary to acute kidney injury Dehydration
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- Cerebraler Blutfluss, diagnostische Veränderungen Normaler cerebraler Blutfluss: 54 ml/100 g/min At 30-40 ml/100 g/min causes EEG changes: The EEG changes that suggest poor prognosis are low voltage, poorly reactive rhythms, periodic lateralised epileptiform discharges and fluctuations in underlying rhythms When the blood flow decreases to 20 ml/100 g/min lactate levels increase. Between 20 ml/100 g/min - 10 ml/100 g/min free radicals are released and evoked potentials begin to disappear. At flow rates lesser than 10 ml/100 g/min irreversible damage occurs due to water accumulation.
- Diurese nach 1 l 20% Albumin beim Gesunden Basic assumptions are: Total body water (TBW) is one third extracellular fluid (ECF) and two thirds intracellular fluid (ICF) ECF is one quarter plasma and three quarters interstitial fluid (ISF) The threshold of the volume receptors in the atria is 7-10% blood volume change The osmoreceptors are sensitive to a 1-2% change in osmolality Plasma osmolality normal prior to the transfusion is likely to be 287-290 mOsm/kg Plasma protein solution is a colloid and is distributed only to the intravascular compartment. The tonicity is unaltered. The blood volume increases from 5,000 mls to 6,000 mls; an increase of 20%. This is above the 7 to 10% threshold for the volume receptors. The secretion of atrial natriuretic peptide (ANP) has the following renal effects: Dilates the afferent glomerular arteriole, constricts the efferent glomerular arteriole, and relaxes the mesangial cells thereby increasing glomerular filtration rate Decreases sodium reabsorption in the distal convoluted tubule and collecting ducts Inhibition of renin release Increased blood flow in the vasa recta. The plasma osmolality is unlikely to change and therefore not affect hypothalamic osmoreceptors.
- Compliance Static Compliance (Cstat) Static compliance represents pulmonary compliance during periods without gas flow, such as during an inspiratory pause. It can be calculated with the formula: where Pplat = plateau pressure. Pplat is measured at the end of inhalation and prior to exhalation using an inspiratory hold maneuver. During this maneuver, airflow is transiently (~0.5 sec) discontinued, which eliminates the effects of airway resistance. The normal compliance (Cl) of a normal lung (adult) is 200 ml/cmH2O; newborn 5 mL/cmH2O. Dynamic Compliance (Cdyn) Dynamic compliance represents pulmonary compliance during periods of gas flow, such as during active inspiration. Dynamic compliance is always less than or equal to static lung compliance. It can be calculated using the following equation, where Cdyn = Dynamic compliance; VT = tidal volume; PIP = Peak inspiratory pressure; PEEP = Positive End Expiratory Pressure: where PIP = peak inspiratory pressure (the maximum pressure during inspiration). Alterations in airway resistance, lung compliance and chest wall compliance influence Cdyn. Dynamic (not static) compliance is related to airways resistance. Specific compliance allows comparison to be made between patients with varying body sizes. total static compliance (lung and chest wall): 100 ml/ cmH2O (mehr Widerstand > kleinere Comliance) Intrapleural pressure can be measured indirectly using an oesophageal manometer. Respiratory volumes can be measured at the mouth using a pneumotachograph.
- Totraum physiologischer Totraum = alveolärer Totraum + anatomischer Totraum = 2-3 ml/ kg (30% des Tidalvolumens) Die Größe des funktionellen Totraums kann mithilfe der Bohr-Formel berechnet werden: VD/VT= PaCO2 - PECO2/PaCO2 (PE: CO2 in Ausatemluft) Fowler's Methode misst anatomischen Totraum. Hierbei nimmt die zu untersuchende Person einen tiefen Atemzug reinen Sauerstoffs, so dass der gesamte anatomische Totraum ausschließlich mit Sauerstoff gefüllt ist. Während der anschließenden Ausatmung wird die Stickstoffkonzentration in der ausgeatmeten Luft gemessen. Zu Beginn der Ausatmung beträgt die Stickstoffkonzentration Null, da zunächst nur aus dem anatomischen Totraum ausgeatmet wird. Bei weiterer Ausatmung steigt sie aber an, da die Alveolarluft noch Stickstoff enthält, und erreicht schließlich ein Plateau, welches der Stickstoffkonzentration in der Alveolarluft entspricht. Das ausgeatmete Volumen, bei dem die Stickstoffkonzentration etwa 50 % des Plateauwertes erreicht hat, entspricht annähernd dem anatomischen Totraum. Totraum-Verhältniss altersunabhängig ratio of dead space (Vd)/ tidal volume (Vt) = 0,3
- Muskarin- Rezeptoren Muscarinic acetylcholine (ACh) receptors: M1-M5 Receptor agonists and acetylcholine cause the activation of various guanosine nucleotide binding proteins (G-proteins). M1, M3, M5 receptors are coupled to phospholipase C M2 and M4 receptors inhibit adenylyl cyclase M1 (predominate in the human brain) and M2 (mainly in the heart). The side effects are a consequence of stimulation of effector organs of the parasympathetic system and at sweat glands of the sympathetic system. They include: Nausea and vomiting Parkinsonism Sweating Cutaneous flushing Diarrhoea Hypotension Bradycardia Bronchoconstriction Urinary bladder contraction.
- Okulokardialer Reflex • Auslösung durch Zug an Augenmuskeln oder Druck auf das Auge (bes. häufig bei Schiel-Op.) Trigemino-(ophthalmico-)vagaler Reflex mit bradykarden Herzrhythmusstörungen → AV-Block → Asystolie • Therapie: Unterbrechung des chirurgischen Reizes, evtl. Atropin Afferenz: parasympatische Nervenfasern der Nn. ciliares und des N. ophthalmicus aus dem Ganglion Gasseri/trigeminus Efferenz: Nucleus ambiguus - N. vagus
- Lunge: Aufgaben main function: gas exchange synthesis of surfactant, prostaglandins and histamine Activation and deactivation of angiotensin, bradykinin, 5-hydroxytryptamine and the handling of amide local anaesthetics blood reservoir: pulmonary circulation contains up to 900 ml of blood and this volume increases by up to 400 ml when in the supine position. Substances are filtered from the pulmonary circulation, for example, thrombus and air; the mucous lining the air passages also traps particles.
- PEEP Although positive end expiratory pressure (PEEP) may provide an oxygen sparing effect by reducing the intrapulmonary shunt and increasing alveolar recruitment it has many deleterious effects including: Decreasing cardiac output Increasing pulmonary artery pressure due to increased pulmonary vascular resistance Increasing dead space Increasing the distension of uninjured lung units increases the risk of barotrauma Increasing extra-vascular lung water by decreasing pulmonary interstitial lymph drainage (although PEEP reduces oedema in left ventricular failure and in fluid overload). The protective effects of PEEP on the lung are mediated not only through its ability to decrease the inspired oxygen requirements, but also due to a reduction in repeated alveolar collapse and re-inflation. This limits the shear stress on the alveolar wall, which reduces the formation of pro-inflammatory mediators by the pulmonary vascular epithelium and alveolar macrophages.
- Plasmaosmolarität Osmolarity is the measure of solute concentration defined as the number of osmoles (Osm) of solute per litre (l) of solution (Osmol/l). Calculated osmolarity = 2 (Na + K) + Glucose + Urea (all in mmol/L). Normal serum osmolarity is 285-295 mOsm/l. Osmolarity can be affected by temperature and pressure and for a given solution this calculated variable is less than the osmolality. Osmolality is also a measure of solute concentration but is defined as the number of osmoles (Osm) of solute per kilogram (Osm/Kg). The value is independent of temperature and pressure. It is measured in the laboratory using an osmometer.
- Lungencompliance Static lung compliance is the change in volume for any given change in pressure. Static compliance is measured at a period when there is no gas flow, for example during an inspiratory or expiratory pause. Compliance = ΔV/ΔP The units are ml/cmH2O or L/cmH2O. Intrapleural pressure can be measured indirectly using an oesophageal manometer. Respiratory volumes can be measured at the mouth using a pneumotachograph or spirometer. The normal compliance (Cl) of a normal lung is 200 ml/cmH2O. For example, if a patient inhales 600 mL of air from a spirometer with an intrapleural pressure before inspiration of -6 cm H2O and -12 cm H2O at the end of inspiration. Cl = 600mL/-6 -(-12)cmH2O = 600/6 = 100ml/cmH2O. In this example with a ventilated patient the static compliance represents pulmonary compliance during periods without gas flow, such as during an inspiratory pause. It can be calculated with the formula: Cstat = Vt/(Pplateau-PEEP) where: Vt = tidal volume Pplateau = plateau pressure PEEP = peak end-expiratory pressure.
- Lungenfunktionsprüfung Atemzugvolumen(AZV) Es entspricht dem ein- bzw. ausgeatmeten Volumen bei normalem Atemzug (etwa 0,5 Liter Luft). Inspiratorisches Reservevolumen(IRV) Dies ist das Volumen, das nach normaler Einatmung noch zusätzlich eingeatmet werden kann (etwa 3 Liter Luft). Expiratorisches Reservevolumen(ERV) Es ist das Volumen, das nach normaler Ausatmung noch zusätzlich ausgeatmet werden kann (etwa 1,7 Liter Luft). Inspiratorische Kapazität (IC) Sie ist definiert als das Volumen, das nach normalem Ausatmen maximal eingeatmet werden kann (etwa 3,5 Liter Luft). Vitalkapazität (VC) Das ist das Volumen, das nach maximaler Einatmung maximal ausgeatmet werden kann (3,3 bis 4,9 Liter Luft). Einsekundenkapazität(FEV1, Tiffeneau-Test) So wird das Volumen bezeichnet, das bei maximaler Einatmung in einer Sekunde maximal ausgeatmet werden kann (min. 70 Prozent der Vitalkapazität); Peak-Flow (Peak-Expiratory-Flow, PEF) Beschreibt den stärksten aus den Lungen ausgestoßene Luftstrom am Beginn einer starken Ausatmung (max. 600 l/min) Functional residual capacity (FRC) is 30 ml per kg. capacity is the sum of two or more volumes. Total lung capacity (TLC) equals the vital capacity (VC) and the residual volume (not FRC). residual volume (RV) can be measured using a body plethysmograph and using the helium dilution technique. CC: In a patient with a normal body mass index and without lung-associated pathology, the closing capacity (CC) equals the FRC in the supine position at the age of 40 years. At 65 years the CC equals the FRC when standing. Closing volume: during active emptying of the lungs airways close off long before residual volume is reached: the point at which this begins to occur is known as the closing volume Closing capacity: closing volume plus the residual volume
- arterial-venous oxygen (a-vO2) difference At rest 70-80% of the oxygen available to the cardiac muscle is extracted and during exercise this might increase to 90% OrganCaO2-CvO2 (volume% or ml O2/100 ml blood) Heart 10-13 Resting skeletal muscle 2-5 Kidney 2-3 Intestine 4-6 Skin 1-2
- Zyanose more than 5 g/dl of reduced haemoglobin arterial saturation is below 85%. It is associated with the following: Congenital heart disease Respiratory disease methaemoglobinaemia sickle cell disease ( "acute chest syndrome" characterised by a vaso-occlusive crisis of the pulmonary vasculature resulting in severe V/Q mismatch and hypoxia.)
- Neugeborene- Lungen- und Herzphysiologie The cardiovascular and respiratory systems of the neonate have the following features: Increases in cardiac output are dependent on changes in heart rate, as the capacity to increase the stroke volume is limited. The average systolic blood pressure in a full term neonate is about 80 mmHg. The pulmonary vascular resistance is high at birth but then falls rapidly in the first few days. In the fetal circulation the high pulmonary vascular resistance results in blood being diverted into the systemic circulation via the ductus arteriosus. The ductus arteriosus usually fibroses within 4 weeks of birth.
- Schlaf Sleep is a naturally occurring state of unconsciousness from which the subject may be easily roused. It has two distinct patterns: Non-rapid eye movement (NREM) sleep and Rapid eye movement (REM) sleep. NREM sleep has four recognised stages. In a typical night a young adult will pass through NREM sleep into REM, and then repeat this cycle several times. Thus, approximately 25% of total sleep time will be spent in REM sleep (not 15%). Opioids decrease stages 3 and 4 of NREM sleep, whereas barbiturates and amphetamines inhibit REM sleep. Catecholamines increase wakefulness (not NREM sleep).
- Schmerzmodulation The dorsal horn is the site where primary afferents terminate, and there is a complex interaction between these afferent fibres, local intrinsic spinal neurones and descending fibres from the brain. A number of substances (peptides, catecholamines and indoleamines) have been implicated as neurotransmitters at the dorsal horn, and when released they modulate peripheral nociceptive input. They include: Substance P Serotonin Noradrenaline Acetylcholine Glutamate Adenosine. Reflex activity also modulates peripheral nociception.
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- MET This patient's calculated VO2 is 3.5 × 50 × 8 = 1400 ml/kg/minute. 1 MET = consumption of 3.5 ml O2/kg/minute. 1 MET EatingDressingUse toiletWalking slowly on level ground at 2-3 mph 2 METs Playing a musical instrumentWalking indoors around houseLight housework 4 METs Climbing a flight of stairsWalking up hillRunning a short distanceHeavy housework, scrubbing floors, moving heavy furnitureWalking on level ground at 4 mphRecreational activity, e.g. golf, bowling, dancing, tennis 6 METs Leisurely swimmingLeisurely cycling along the flat (8-10 mph) 8 METs Cycling along the flat (10-14 mph)Basketball game 10 METs Moderate to hard swimmingCompetitive footballFast cycling (14-16 mph)
- Valsalva- 4 Phasen The Valsalva manoeuvre involves forced expiration against a closed glottis to generate an intrathoracic pressure of 40 mmHg for 10 seconds. The effects on the heart rate (HR) and blood pressure (BP) are then monitored and divided into four phases. Phase I - An initial increase in venous return from intrathoracic vessels causes a transient decrease in HR and increase in BP. Phase II - As the high intrathoracic pressure in maintained there is a decrease in the venous return which is sensed by baroreceptors. This causes an increase in HR and decrease in BP. The BP tends to return to normal by the end of phase II. Phase III - Sudden release of forced expiration and/or glottal opening results in a return of the intrathoracic pressure to normal. This causes pooling of blood into intrathoracic vessels resulting in a decrease in BP, whilst the HR remains elevated. Phase IV - During phase IV the intrathoracic pressure remains normal and the continued increase return of systemic venous blood produces a reflex bradycardia associated with an increase in BP to normal.
- Autoregulation The coronary, renal and cerebral circulations are capable of autoregulation. Niere: Autoregulation is the ability of a vascular bed to maintain perfusion despite fluctuations in systemic arterial pressure. The renal blood flow can be maintained between a mean arterial pressure (MAP) of 80 mmHg and 180 mmHg. There are two main mechanisms of renal autoregulation, these are: Myogenic response; is the function of vascular smooth muscle to contract in response of a stretching force. This is thought to be due to an influx of Ca2+ into the myocytes activated by stretch dependent voltage-gated ion channels. Tubuloglomerular feedback (TGF); this mechanism leads to the constriction of the pre-glomerularafferent arterioles in response to an increase in luminal concentrations of Na+ in the macula densa of the distal convoluted tubule. An increase in arterial pressure will enhance tubular flow and improved glomerular filtration rate and reduced proximal tubular reabsorption. Renal autoregulation minimises the impact of changes in arterial blood pressure on Na+ excretion. Autoregulation is well preserved in denervated kidneys. The effect of a fall in mean arterial pressure to the range 80-100 mmHg is likely to cause an increase in renal blood flow and a fall in renal vascular resistance.
- Oxygen reserve CompartmentFactorsRoom air (mL)100% O2 (mL) Lung FAO2, FRC 630 2850 Plasma PaO2, DF, PV 7 45 Red blood cells Hb, TGV, SaO2 788 805 Myoglobin 200 200 Interstitial space 25 160 FAO2 alveolar fraction of oxygen rises to 95% after administration of 100% oxygen (CO2 = 5%) FRC 2,500-3,000 mL in medium sized adults PaO2 partial pressure of oxygen dissolved in arterial blood (80 mmHg breathing room air and 500 mmHg breathing 100% oxygen) DF dissolved form (0.3%) PV plasma volume (3L) TG total globular volume (5L) Hb haemoglobin concentration SaO2 arterial oxygen concentration (98% breathing air and 100% when preoxygenated)
- Hyponatriämie It occurs in: Acute renal failure due to volume overload Hypothyroidism and Following prolonged infusions with oxytocin, which has mild antidiuretic hormone (ADH) activity. Water intoxication and hyponatraemia may cause problems during labour especially if prolonged infusion has been given in addition to intravenous fluids.
- Shunt Physiological shunt: normally 2-4% of the cardiac output bypasses the lungs. Coronary arterial blood empties directly into the left ventricle via the thebesian veins Some bronchial arterial blood empties directly into the pulmonary veins. Pathological shunt: Congenital heart disease with right to left shunt Perfusion of non-ventilated areas of lung (V/Q ratio = zero). For example, areas of atelectasis or bronchial obstruction Pulmonary arterio-venous shunts.
- ventilation/perfusion (V/Q) relationships in the lung The ideal V/Q ratio is 0.8 because normal cardiac output is 5 l/min and normal alveolar ventilation is 4 l/min. In the lateral position the perfusion of the dependant lung increases are greater than the compliance and ventilation of the dependant lung. The lung is generally classified into three zones: Zone 1: PA>Pa>PV; represents alveolar dead space; top of lungs Zone 2: Pa>PA>PV; middle of the lungs Zone 3: Pa>PV>PA ; bottom of the lungs. Extreme variations of V/Q: Areas with no ventilation but some perfusion (V/Q = zero or shunt).Areas with no perfusion but some ventilation (V/Q = infinity or dead-space). At the apex of an upright lung V/Q = 3.3. PaO2 increases and PaCO2 decreases. Ventilation is "wasted" compared with perfusion. At the bases of the lung V/Q = 0.67 There will be impairment of gas exchange. PaO2 falls and PaCO2 increases. Overall the V/Q ratio is 0.8. The PO2 at the apex of the lung is 132 mmHg compared with PO2 89 mmHg at the base. The calculated pH is higher (more alkaline) at the top of the lung compared with the base (7.51 at the apex and 7.39 at the base), and this is a reflection of the higher PCO2 at the base of the lung.
- Closing capacity Closing capacity is the lung volume at which small airways in the dependent parts of the lung begin to close. It equals the closing volume plus the residual volume. In young adults the closing capacity (CC) is less than the functional residual capacity (FRC), but it equals and then exceeds it with increasing age (from middle age onwards). At 40 years the CC equals the FRC in the supine position and at 65 years the CC equals the FRC when standing. When CC exceeds the FRC, airway closure and a ventilation/perfusion mismatch occurs during normal tidal ventilation, and is an important cause of hypoxaemia. Thus, CC increases with age (not decreases); CC decreases with the onset of anaesthesia; but it is unaffected by changes in body position. However, factors that reduce FRC may result in the CC encroaching upon the FRC which will cause airway closure. CC is measured using the nitrogen single breath test: From full expiration (residual volume) the patient inhales to total lung capacity (TLC) and then exhales slowly. The lung volume at which the dependent airways start to close (i.e. closing capacity) is indicated by an increase in the concentration of exhaled nitrogen. Helium and other marker gases may also be used.
- restriktive Ventilationsstörung Restrictive lung disease occurs when the lungs or the structures that surround them (pleura, rib cage or abdomen) limit the expansion of the lungs in a volume dependent fashion. These include: Interstitial abnormalities (pulmonary oedema, inflammation) Collapse or consolidation of alveoli, or External compression of the lungs (ascites, pneumothorax). As a consequence There is increased muscular effort to maintain tidal volume Alveolar volume decreases so there is Decreased functional residual capacity Arterial PO2 decreases and there is Arterial hypoxaemia causing increased respiratory drive. Because there is no obstructive defect, the slope of the forced expiratory curve is initially normal, until limited by the restrictive nature of the defect. The FEV1 may, therefore, be reduced, but the FEV1/2 is unlikely to be significantly down. Total lung capacity is usually severely reduced. Tidal volume may be normal, but there will be decreased respiratory reserve. Peak flow is usually reduced.
- Total lung capacity Total lung capacity equals the vital capacity plus the residual volume and is a specific measure of lung size. It is therefore decreased in most lung abnormalities but does not depend on the thickness of the alveolar wall. In cystic fibrosis there are areas of overinflation, but also areas of atelectasis, so the overall lung volume is reduced (not increased). It is reduced in severe cerebral palsy. In the helium dilution technique, the change in concentration of a known volume of helium is used to estimate the total lung capacity following equilibration.
- Cardiac output MAP = CO × SVR. CO reduziert durch: Sleeping (reduced metabolic requirements) Abnahme der Körpertemperatur (reduced metabolic requirements) Initial: Aufstehen aus dem Liegen (Reduktion Vorlast) CO erhöht durch: Histamin > Vasodilatation with reduced left ventricular end-diastolic pressure and stroke index. To compensate there is an increase in heart rate, cardiac output and LV dP/dt max. However, in anaphylaxis, the changes resulting from massive histamine release overwhelm the cardiac regulatory mechanisms leading to a net reduction in cardiac output and cardiac arrest may occur. Post-prandially cardiac output is increased by 30%.
- Zyanose Central cyanosis is usually detectable once the oxygen saturation drops below about 80-85%. Cyanosis occurs with presence of >5 g/dl of reduced haemoglobin. It is, therefore, not detectable in patients with severe anaemia, even if they are gravely hypoxaemic. It may be respiratory or cardiac in origin. Occasionally, cyanosis can be because of abnormal pigments such as sulphaemoglobin or methaemoglobin. In these cases arterial oxygen tension is often normal. Two types of methaemoglobinämie occur, Genetic (asymptomatic) Acquired (due to ingestion of oxidant drugs, for example, analine dyes, GTN, dapsone, which give symptoms of anaemia with or without haemolysis). Sulphaemoglobin is usually acquired by ingestion of sulphonamides or phenacetin.
- ABGA: Normwerte pH = 7,35–7,45 pO2 = 75–97 mm Hg bzw. 10–12,9 kPa (je nach Alter) saO2 = 95–99 % pCO2 = 35–45 mm/ 4,6-6,0 kPa HCO3(act) = 21–26 mmol/l (aktuelles Bicarbonat) HCO3(std) = 23–27 mmol/l (Standard–Bicarbonat) BE = 0 mval/l (-2 bis +3 mmol/l)
- Höhe (Mount Everest):8400 m arterial partial pressures of oxygen is less than 4 kPa Atmospheric pressure one third that at sea level, about 34 kPa.2 The boiling point of a substance is the temperature at which the vapour pressure of the liquid equals the pressure above the liquid. Therefore, as atmospheric pressure falls with increasing altitude so does the boiling point. inspired oxygen is still 0.21 but the partial pressure of oxygen is about 7.1 kPa (compared to about 21.2 kPa at sea level). Saturated vapour pressure is a function of temperature. Therefore, at constant temperature, saturated vapour pressure is constant.
- Blutvolumen Kind 80 ml/kgKG
- Körperwasser is subdivided into: Extracellular fluid (ECF) = (1/3) Intracellular fluid (ICF) = (2/3) The ECF volume is subdivided into: Interstitial fluid = 3/4 litres Plasma = 1/4,litres Transcellular fluid (CSF/synovial fluid) = wenig Fluid compartments directly measured: Total body water can be measured using heavy water (deuterium), which is freely distributed. Plasma volume can be measured by labelling albumin with a radioactive isotope or using a dye called Evans blue. They remain in the plasma and do not diffuse into erythrocytes. Total erythrocyte volume can be measured using radiolabelled (Cr-51) red blood cells. ECF volume can be measured using inulin as the tracer as it is freely distributed to the interstitial and plasma volumes. Fluid compartments indirectly measured: Total blood volume can be calculated with knowledge of the haematocrit and the total circulating red cell volume. ICF volume can be calculated by subtracting ECF volume from measured TBW.
- NO Nitric oxide (NO) is synthesised in endothelial cells (not epithelial) by the oxidation of L-arginine to L-citrulline, and the reaction is catalysed by nitric oxide synthetase. NO diffuses into vascular smooth muscle activating guanylate cyclase, which converts GTP into cyclic GMP, resulting in relaxation (not cyclic AMP). It has a biological half life of four to 40 seconds, and its action is terminated by combining with haemoglobin to form methaemoglobin. In sepsis NO production is increased by endotoxin.
- Neurotransmitter Epinephrine (adrenaline) produces vasodilatation of arterioles within skeletal muscles but constriction of other vessels. Norepinephrine (noradrenaline) causes marked vasoconstriction. A decreased PO2 produces vasodilatation, but serotonin (or 5HT) generally causes vasoconstriction except for vasodilatation within muscle arterioles.
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