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179 Cards in this Set
- Front
- Back
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Tidal volume:
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volume of each breath
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Minute ventilation:
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volume of air breathed per minute (tidal volume (VT) x respiration refquency (f))
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Distribution of tidal volume:
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alveolar ventilation (VA) and dead space ventilation (VD)
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Location of dead space ventilation:
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conducting airways (no gas exchange occurs), poorly perfused or poorly ventilated alveoli (minimal to no gas exchange can occur)
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Mechanisms of relaxation of airway smooth muscle by inhalant anesthetics:
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inhibition of inward Ca currents through voltage-dependant Ca channels, inhibition of IP3 induced Ca release from the sarcoplasmic reticulum, decreased sensitivity of contractile mechanisms to Ca
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Functional residual capacity:
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volume of air remaining in the lungs at the end of tidal exhalation
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Causes of decrease in functional residual capacity:
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recumbency, effect of anesthetic agent
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Effects of positive pressure ventilation and positive end expiratory pressure on cardiac output:
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decrease by decreasing venous return to the right atrium due to increased intrathoracic pressure
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What factors affect blood flow distribution to the lung:
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CO, posture, lung volume, vascular pressure & resistence, positive pressure ventilation, positive end expiratory pressure, hypoxic pulmonary vasoconstriction
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Causes of alveolar hypoventilation:
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(1) depression of CNS by anesthetic drugs or trauma (2) peripheral nerve injury leading to dysfunction of respiratory muscles (3) depression of cardiac pump by drugs, trauma, compression by bloated abdomen (4) lung resistence due to airway obstruction or decreased lung compliance
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Causes of hyperventilation:
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hypoxic stimulus, acidosis, increased body temperature
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Most important determinant of gas exchange:
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matching of ventilation to blood flow (V/Q matching)
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What occurs with an increased V/Q ratio?
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Dead space ventilation, decreased PaO2 and increased PaCO2
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What occurs with a decreased V/Q ratio?
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Venous admixture, decreased PaO2 and normal or decreased PaCO2
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Sources of hypoxemia:
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hypoventilation, V/Q mismatch, delivery O2 (DO2)/ oxygen uptake imbalance (VO2)
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What factors shift the O2-Hb dissociation curve to the right?
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Increased body temperature, increased PCO2, increased 2,3 diphosphoglycerate, or decreased pH
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What factors shift the O2-Hb dissociation curve to the left?
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Decreased body temperature, decreased PCO2, decreased 2,3 diphosphoglycerate, increased pH
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Formula for calculating arterial O2 concentration:
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CaO2= (1.39 x Hb x SaO2) + 0.03 x PaO2
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Effects of parasympathetic nervous system on the heart:
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inhibitory (muscarinic acetylcholine) by decreasing adenylate cyclase activity, opening K channels, decreasing SA node, slowing AV node, mild decrease in contractility
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Effects of sympathetic nervous system on the heart:
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release of norepinephrine, increase cAMP and activation of Ca channels via B1 resulting in increased HR, increased conduction through AV node, increased force of contraction
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Phases of cardiac cycle:
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Diastole (relaxation and filling) and systole (contraction and ejection of blood)
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Phases of systole:
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isovolumetric contraction (from closure of mitral/ tricuspid valves to opening of aortic/ pulmonary valves), ventricular ejection (from opening of aortic/ pulmonary valves to closure of aortic pulmonary valves), isovolumetric relaxation (from aortic/ pulmonary valve closure to mitral/ tricuspid opening)
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Association of cardiac cycle to heart sounds:
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S1 from closure of the mitral/ tricuspid valves in early systole; S2 from closure of aortic/ pulmonary valves at end systole; S3 from ventricular filling in early diastole; S4 fro atrial contraction at end diastole
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What is the cause of a split S2 heart sound?
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Asynchronous closure of the aortic or pulmonary valves
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Association of cardiac to ECG:
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P wave is atrial depolarization propagated from SA node in end diastole; QRS is depolarization & contraction of ventricles starting in late diastole to early systole; T is ventricular depolarization in end systole
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What does the PQ interval represent?
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Time of conduction from SA node to AV node
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What does the QT interval represent?
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Total electrical depolariazation-repolarization time in the ventricle
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What is stroke volume?
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Difference between end diastole ventricular volume and end systolic ventricular volume
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Define ejection fraction:
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SV/end diastolic volume
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Definition of cardiac output:
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amount of blood pumped by the ventricle in 1 min (L/min)
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Equation for cardiac output:
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SV x HR
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What an estimation of pre-load?
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End diastolic ventricular volume
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Equation for systemic vascular resistance:
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SVR = MAP/CO
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Location of atrioventricular valves:
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tricuspid right atria-ventricle; mitral left atria-ventricle
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What are the determinants of O2 uptake (VO2)?
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CO x O2 extraction (CaO2-CvO2 = difference between O2 content in arterial and venous blood)
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What is the O2 extraction ratio?
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ERO2 = CaO2-CvO2/CaO2 or SaO2-SvO2/SaO2
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Placement of base-apex ECG leads:
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+ over left apex of heart (near left olecranon) – over right jugular furrow
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Most common congenital cardiovascular disease:
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ventricular septal defects, patent ductus arterious (retention of vessel between pulmonary artery and aorta) is rare in horses
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Most common valvular diseases:
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tricuspid or mitral regurgitation, aortic insufficiency
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Causes of valvular insufficiency:
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valvulitis, endocarditis, mitral valve prolapse (rupture cordea tendonea)
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Results of valvular insufficiency:
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ventricular volume overload, increased myocardial demand, heart failure, decreased CO
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Drugs to treat cardiogenic shock:
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dobutamine or dopamine
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Drugs to treat sinus arrest/ bradycardia/ complete AV block:
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atropine, glycopyrrolate, dobutamine, dopamine
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Drugs to treat atrial or supraventricular arrhythmias:
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quinidine, procainamide, digoxin, diltiazem, propranolol
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Drugs to treat atrial fibrillation/ flutter:
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lidocaine, MgSO4, procainamide
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Treatment of atrial fibrillation with quinidine sulfate:
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Place IVC for venous access, place NGT, admin 22mg/kg via NGT q2hrs until (1) conversion (2) signs of toxicity (3) total of 406 doses have been given
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MOA acepromazine (phenothiazines):
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depression of basal ganglia & limbic system, modulating reticular activating system possible by interference with dopamine
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MOA of phenothiazine hypotension:
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depression of hypothalamus, block of peripheral a2 adrenoreceptors, direct vasodilatory effects on vessels
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Examples of benzodiazepines:
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diazepam, midazolam, climazolam
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MOA of benzodiazepines:
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bind to inhibitory GABA receptors in brainstem reticular formation & spinal cord
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Where are a1 adrenoceptors located?
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CNS, heart, smooth muscle, liver
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a1 function in CNS:
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increase awareness & activity
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a1 function in heart:
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increase contractility, sensitive myocardium to catecholamines with halothane
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a1 function in smooth muscle:
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vasoconstriction
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a1 function in liver:
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glyconeogenesis, gluconeogenesis
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Where are a2 adrenoceptors located?
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CNS, SNS, cholinergic neurons, heart, smooth muscle, gut, pancreas, platelets, fat
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a2 function in CNS:
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decrease norepinephrine & dopamine release (sedation, cardio depression)
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a2 function in SNS:
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inhibit norepinephrine release
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a2 function at cholinergic neurons:
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inhibit neuron
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a2 function at heart:
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decrease norepinephrine release
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a2 function in smooth muscle:
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vasoconstriction
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MOA local anesthetic agents:
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enter Na channels & inhibit influx of Na ions of nerve cells
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Local anesthetics ranked by potency & duration:
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lidocaine=meoivicane < ropivacaine < bupivicane
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MOA barbiturates:
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decreased Na, K, Cl or increased Cl ions across cell membranes resulting in depression of reticular activating system; mimic & enhance GABA
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Effects of GABA receptor:
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increased Cl ion conductance (membrane hyperpolarization)
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Side effects of barbiturates:
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unpredictable or inadequate drug effects, apnea
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MOA dissociative anesthetics:
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interaction with NMDA receptors in CNS, interaction with opioid receptors, ketamine also interferes with serotonin, dopamine, GABA
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Side effects of dissociatives:
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failure of adequate anesthesia, short duration of anesthesia, excitement or delirium during recovery, decreased ventilation or apnea
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Effects of large doses of dissociatives:
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direct myocardial depression +/- failure resulting in hypotension, pulmonary edema
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MOA guaifenesin:
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binds inhibitory NT receptors sites activated by GABA
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MOA propofol:
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potentiates GABA induced chloride current by binding GABA
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Why is TIVA limited to short procedures?
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Cumulative drug effects, prolonged time for drug elimination, expense
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What drug can be used for prolonged TIVA?
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Propofol
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MAC:
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minimum alveolar concentration- end alveolar concentration of an inhalation anesthetic that prevents purposeful movement in response to stimulus in 50% of patients
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MAC of common inhalation anesthetics:
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halo 0.9 iso 1.31 sevo 2.31 des 7.02
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Factors that increase MAC:
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hyperthermia, hypernatremia, drugs stimulating CNS
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Factors that decrease MAC:
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hypothermia, hyponatremia, pregnancy, PaO2 < 40mmHg, PaCO2 >95mmHg, increasing age, drugs that depress CNS
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Factors that affect alveolar uptake & elimination of inhalation anesthetics:
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inspired concentration, ventilation, solubility, CO, alveolar to mixed venous partial pressure difference, tissue uptake, tissue capacity & tissue blood flow
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Indications for O2 supplementation:
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hypoxemia (PaO2 < 60mmHg) Hb <5g/dL
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Indications for ventation supplementation:
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apnea, hypoxemia PaO2 <60mmHg, hypoventilation/ hypercapnia PaCO2 >70mmHg, decrease the work of breathing, stabilize inhalant anesthesia, facilitate surgery, administration of neuromuscular bloackade
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Objectives of ventilator support:
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optimize CO2 removal from lungs & deliver O2 to alveoli
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Effects of mild-moderate hypercapnia:
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increase CO, decreased SVR, increased tissue perfusion, modulation of cerebral blood flow (cerebral vasodilation), shift O2 dissociation curve to right, increased tissue oxygenation & availability
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Effects of severe hypercapnia:
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decreased pH, increased K, myocardial depression, SNS activation & catecholamine release (tachycardia, arrhythmias), impairment of enzymatic function, CNS depression
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Effects of positive end expiratory pressure:
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recruits lung units, increased functional lung capacity, reduces shunt, improves PaO2, increases CVP, decreases venous return/ CO/ ABP, increases ICP, may cause barotrauma
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Classes of neuromuscular blocking agents:
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non-depolarizing, depolarizing, faciliatory drugs
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Examples of non-depolarizing neuromuscular blockade:
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atracurium, pancuronium, rocuronium
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Examples of depolarizing neuromuscular blockade:
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succinylcholine
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Examples of faciliatory (reversal) neuromuscular blocking drugs:
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neostigmine, edrophonium
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MOA of non-depolarizing neuromuscular blocking drugs:
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bind to acetylcholine receptors blocking access to Ach
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MOA of depolarizing neuromuscular blocking drugs:
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binds post-synaptic Ach receptors, opens channels, causes depolarization of motor end plate, channel remains open so does not repolarize
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What processes are involved in nociception?
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Transduction, transmission, modulation, projection, perception
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Morphine class of opioid:
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mu agonist
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Fentanyl class of opioid:
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mu agonist
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Butorphanol class of opioid:
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kappa agonist/ mu antagonist
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Methods to improve PaO2:
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increase FiO2, control ventilation, increase CO, change position
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Relation of oxygen consumption in the foal to the adult:
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6-8mL/kg/min in foals which is 2-3 times more than the adult
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How can epinephrine be administered for CPR?
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IV (0.01-0.02 mL/kg), intraosseous (same as IV dose), via endotracheal tube (0.05-0.1 mL/kg diluted in 1-2mL saline)
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What are the consequences of epinephrine administration?
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Ventricular fibrillation, pulseless ventricular tachycardia, increased SVR, all of which increase myocardial O2 demand & workload
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When to myopathies most often occur in association with anesthesia?
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Hypotension > 15 min, anesthesia time > 3 hrs
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Define peripheral sensitization:
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tissue damage results in release of inflammatory mediators which stimulate nerve endings directly or increase sensitivity of the nociceptor to other stimuli
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Define central sensitization:
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NMDA stimulation by glutamate resulting in hyperalgesia and an exaggerated response to noxious stimuli
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What is tramadol?
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Synthetic codeine analogue, binds (weakly) mu receptors and inhibits uptake of norepinephrine & serotonin
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MOA gabapentin:
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unknow but thought to modulate activity of presynaptic voltage gates Ca channels
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Tramadol class of opioid:
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mu agonist
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Drugs that reduced MAC combined with inhaled anesthesia:
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Lidocaine, medetomidine (3.5-5ug/kg/hr), romifidine (0.3 ug/kg/min), ketamine (0.5-1 mg/kg/hr)
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Dose of epidural lidocaine:
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0.22 mg/kg
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Duration of epidural lidocaine:
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1.5 hrs
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Onset of epidural lidocaine:
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4 min
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Dose of epidural bupivacaine:
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0.06 mg/kg
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Duration of epidural bupivacaine:
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5.3 hrs
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Onset of epidural bupivacaine:
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6 min
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Dose of epidural xylazine:
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0.25 mg/kg
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Duration of epidural xlyazine:
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3 hrs
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Onset of epidural xylazine:
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13 min
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Dose of epidural detomidine:
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0.06 mg/kg
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Duration of epidural detomidine:
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2 hr 40 min
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Onset of epidural detomidine:
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12 min
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Dose of epidural morphine:
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0.1 mg/kg
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Duration of epidural morphine:
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6 hrs
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Onset of epidural morphine:
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5 hrs
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Dose of epidural ketamine:
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0.5-2 mg/kg
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Duration of epidural ketamine:
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30-75 min
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Onset of epidural ketamine:
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5-10 min
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Dose of epidural lidocaine + xylazine:
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0.22 mg/kg lidocaine, 0.17 mg/kg xylazine
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Duration of epidural lidocaine + xylazine:
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5hrs 30 min
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Onset of epidural lidocaine + xylazine:
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5 min
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Eye position & reflexes in light plane of anesthesia (1):
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small pupil, ventromedial position, mildly depressed palpebral reflex, active corneal reflex
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Eye position & reflexes in medium plane of anesthesia(2):
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medium pupil size, ventromedial position, depressed palpebral, mildly depressed corneal reflex
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Eye position & reflexes in medium-deep plane of anesthesia (3):
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medium pupil size, central position, depressed palpebral and corneal reflexes
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Eye position & reflexes in deep plane of anesthesia (4):
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pupil large, central position, absent palpebral, markedly depressed corneal reflex
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Anesthesia for foal with ruptured bladder:
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problems are metabolic acidosis, hypoglycemia and hyperkalemia, add CaCl (0.2 mL/kg) or Ca gluconate to BES, treated acidosis (ph<7.2) with NaHCO3 (1mEq/kg), add 4-5 mg/kg/min glucose while monitoring glucose
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Oxygen flow rate:
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initially 8-12 L/min then can decrease to low flow 2.2 mL/kg (low flow system)
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Activity of epinephrine:
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B1=B2> a
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Epinephrine effect on CO:
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large increase
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Epinephrine effect on ABP:
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increase
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Epinephrine effect on HR:
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large increase
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Epinephrine effect on vasoconstriction:
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increase
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Epinephrine effect on arrhythmias:
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very large increase
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Epinephrine effect on diuresis:
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none
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Activity of dobutamine:
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B1>B2>a
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Dobutamine effect of CO:
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large increase
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Dobutamine effect on ABP:
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increase
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Dobutamine effect on HR:
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none to increase
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Dobutamine effect on vasoconstriction:
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increase with high doses
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Dobutamine effect on arrhythmias:
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large increase
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Dobutamine effect on diuresis:
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none
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Activity of dopamine:
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dopamine receptor > B, has a with increased dose
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Dopamine effect on CO:
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large increase
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Dopamine effect on ABP:
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increase with high doses
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Dopamine effect on HR:
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increase
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Dopamine effect on vasoconstriction:
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increase
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Dopamine effect on arrhythmias:
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increased with high dose
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Dopamine effect on diuresis:
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large increase
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Activity of ephedrine:
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a > or equal to B
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Ephedrine effect on CO:
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increase
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Ephedrine effect on ABP:
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increase
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Ephedrine effect on HR:
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none to increase
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Ephedrine effect on vasoconstriction:
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increase
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Ephedrine effect on arrhythmias:
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increase
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Ephedrine effect on diuresis:
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increase
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Activity of norepinephrine:
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B1 > a >B2
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NOR effect on CO:
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none to increase
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NOR effect on ABP:
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large increase
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NOR effect on HR:
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increase
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NOR effect on vasoconstriction:
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large increase
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NOR effect on arrhythmias:
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increase
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NOR effect on diuresis:
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increase
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Activity of phenylephrine:
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a
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Phenylephrine effect on CO:
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none
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Phenylephrine effect on ABP:
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very large increase
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Phenylephrine effect on HR:
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none
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Phenylephrine effect on vasoconstriction:
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very large increase
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Phenylephrine effect on arrhythmias:
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none
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Phenylephrine effect on diuresis:
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decrease
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Effects or uses of anticholinergic drugs (examples of drugs):
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atropine & glycopyrolate are used to prevent vagal induced bradycardia, reduce respiratory secretions, produce bronchodilation
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Ventilator inspiration:expiration ratios:
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adults 1:2 or 1:3, foals 1:3
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Ventilator inspiratory time:
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adult 2-3 seconds, foal 2 seconds
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Relationship between ETCO2 and PaCO2:
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in theory, should be equal but ETCO2 tends to be 10-15mmHg lower than PaCO2
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What influences the ETCO2-PaCO2 difference?
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Ventilation, body position, increases with length of anesthesia or a decrease in CO
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