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223 Cards in this Set
- Front
- Back
what is the purpose of Nasopharyngeal /Oropharyngeal airways
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to keep upper airway open
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what are some indications for an artificial airway
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Respiratory Failure for any reason:
Failure to breath Hypoxemia Hypercapnea Airway Obstruction for any reason /Need for assisted airway clearance or lost ability to protect airway: Trauma, inhalation injury, infection, fire, allergy, hematoma, tumor, congenital, OD, cardiac arrest, surgery, CVA, decreased LOC, head injury,Surgery |
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what happens if your trach tube is too short
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tongue will occlude
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what are the indications for a combi tube
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Assistance with ventilation not just to open airway
Skill level available for insertion No upper airway obstruction |
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what is a combitube
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Trach tube bonded with esophageal obturator
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where is the distal tube and what does it do
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inflates in the esophagus. isolates the laryngopharnx from the esophagus
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what does the proximal tube do
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inflates at the base of the tongue. isolates the larngopharnixs from the oropharnyx and the nasopharnyx
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what are the indications for an endo tube
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Assistance with ventilation not just to open airway
Skill level available for insertion No upper airway obstruction |
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what are the types of endo tubes
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Orotracheal/nasotracheal
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what is the difference between Orotracheal/nasotracheal
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O=easy access, bigger tube
N=easily secured, better tolerated, no head flexion needed |
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when do you see difficult intubation
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decreased C-spine mobility
decreased Mouth opening (< 2 fingerbreadths) Distance from thyroid to mandible < 3 fingerbreadths High arched palate - Mallampati class 2 or more. |
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what are the Consequences of esophageal intubation
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catastrophic cerebral hypoxia.
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what do you do post intubation
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5 point auscultation-auscultation over the stomach (left upper quadrant) and bilateral lung fields.
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what color does the CO2 paper turn when CO2 is present
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changes from purple to yellow
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what is sulfonephthalein
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impregnated pH-sensitive filter paper as an indicator that changes from purple to yellow in the presence of carbon dioxide.
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what are the Consequences of inappropriate placement
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Esophageal intubation
Right (or left) mainstem intubation |
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how do you assess tube position
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Bilateral CW movement carefull see below
Bilateral breath sounds No stomach movement/distention Mist in tube CO2 detector changes color SaO2 improves |
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what are the advantages of a trach
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Upper airway bypass
Long term vent Communication Eat Comfort decreased WOB |
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what are the disadvantages of a trach
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Skill
Aspiration risk surgical complications accidental dislodgment infection bleeding |
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what happens if there is too much pressure on a cuff
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Excessive tracheal wall pressure
Interruption cilia escalator Edema Scarring malacia TE fistula Tracheal-innominate artery fistula |
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what is the Minimal leak technique
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hear small leak on inspiration ..Peep/aspiration problems
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what is the minimal occlusive technique
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No leak at peak inspiration
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what is the herniation of the cuff
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over the lumen of the tube may occur if the cuff of an old, perished tube is over-inflated
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what are the complications of inserting an artificial airway
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Hypoxemia…
Aspiration… damage teeth… trauma of tissues, cardiovascular problems… |
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what can cause a tube occlusion
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Biting…
Balloon herniation.. Mucus plug…. |
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what are the immediate complications following extubation or decannulaiton
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1. Aspiration
2. Laryngospasm 3. Laryngeal edema |
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what are the long term complications following extubation or decannulaiton
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1. Sore throat/ Ulcerations
2. Tongue numb (hypoglossal nerve) 3. Vocal cord paralysis 4. Laryngeal granuloma (web) 5. Tracheal stenosis |
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how is central airway plugging treated
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Aggressive hydration
Antibiotic Steroids Guiafensin (gwye fen' e sin) Acetylcysteine (Mucomyst) Inhaled dornase (DOR-nayse ) cystic fibrosis kid |
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what is acute respiratory failure
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Rapid failure of pulmonary system to maintain oxygen or carbon dioxide balance
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what is hypoxemia
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PaO2 less than 60
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what is hypercarbia
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PaCO2 greater than 55
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what is excitability
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cell can be electrically stimulated
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what is contractility
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cell can respond mechanically to an impulse
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what is conductivity
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cell can transmit an impulse along a membrane in an orderly manner
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what is automatcity
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cell can initiate impulse regularly and spontaneously (even non-pacemaker cells)
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what is the absolute refractory period
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Excitability is zero
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what is a relative refractory period
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occurs after ARP for a shorter period of time) Excitability is more likely and if occurs, can cause fibrillation of ventricles
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what is an action potential
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Stimulation of a cardiac cell causes a change in electrical potential of the cell membrane
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what is phase 4 of the action potential
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it is the resting membrane potential - the cell is not being stimulated
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what happens in phases 0-3 of the action potential
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The cell is electrically stimulated - typically by an electric current from an adjacent cell),
There is an influx and efflux of multiple cations and anions that together produce the action potential of the cell, propagating the electrical stimulation to the cells that lie adjacent to it. |
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what is the polarized state of the cell
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There is a high concentration of sodium and low concentration of potassium outside the cell
There is a high concentration of potassium and low concentration of sodium inside the cell Inside of the cell is negative compared to the outside |
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what is depolarization
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When stimulated, the cell membrane becomes permeable to sodium & calcium allowing them to migrate rapidly into the cell
Inside of the cell becomes more positive than outside of the cell |
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what does depolarization cause
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the muscle to contract
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what is repolarization
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Slower movement of ions across the membrane which restores the membrane to the polarized state.
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what are the initial symptoms of ARF
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Change in LOC
RR less than………RR greater than… HR … BP….. Use of accessory muscles Anxiety C/O “shortness of breath”…”something is wrong |
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what does cholinergic mean
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nerves that are stimulated by acetylcholine. Parasympathetic stimulation
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what does adrenergic mean
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activated by adrenalin (norepinephrine), sympathetic nervous system
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what does symptholytic mean
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antiadrenergic. Opposite effects of the impulses conveyed by stimulation of the sympathetic nervous system
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what does chronotropic mean
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affecting the time or rate
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what odes inotropic mean
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affecting the contraction of muscles
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what does dromotropic mean
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an agent that influences the conduction of electrical impulses. A positive dromotropic agent enhances the conduction of electrical impulses to the heart.
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what is a vasopressor
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Producing constriction of the blood vessels and a consequent rise in blood pressure.
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what is a vasodilator
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An agent, such as a nerve or hormone, that widens the blood vessels, which in turn decreases resistance to blood flow and lowers blood pressure.
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what is a catecholamine
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any of a group of sympathomimetic amines (including dopamine, epinephrine, and norepinephrine), the aromatic portion of whose molecule is catechol.
The catecholamines play an important role in the body's physiological response to stress. Their release at sympathetic nerve endings increases the rate and force of muscular contraction of the heart, thereby increasing cardiac output; constricts peripheral blood vessels, resulting in elevated blood pressure; elevates blood glucose levels by hepatic and skeletal muscle glycogenolysis; and promotes an increase in blood lipids by increasing the catabolism of fats. |
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is epinephrine an arterial vasodilator, venous vasodilator, or vasopressor
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vasopressor
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is dobutamine an arterial vasodilator, venous vasodilator, or vasopressor
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vasopressor
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is norepinephrine an arterial vasodilator, venous vasodilator, or vasopressor
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vasopressor
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is phenylphrine an arterial vasodilator, venous vasodilator, or vasopressor
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vasopressor
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is nipride an arterial vasodilator, venous vasodilator, or vasopressor
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mixed arterial and venous dilator
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is vasopressin an arterial vasodilator, venous vasodilator, or vasopressor
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vasopressor
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is nitroglycerin an arterial vasodilator, venous vasodilator, or vasopressor
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mixed arterial and venous dilation
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what does anaerobic metabolism cause
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97% less atp formed, lactic acid is formed, cellular death, acidosis, multiple organ dysfunction.
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what are the main positive ions
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sodium, potassium and calcium
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what is the main negative ion
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chloride
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if we are dead, the concentration of ions on both sides of the cell wall would be what
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equal
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what happens in phases 0-3 of the action potential
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the cell is electrically stimulated and there is an influx and efflux of multiple cations and anions that together produce the action potential of the cell, propagating the electrical stimulation to the cells that lie adjacent to it
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what is the result of phases 0-3
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an electrical stimulation conducted from one cell to all the cells that are adjacent to it, to all the cells of the heart
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phases 0-3 of the action potential cause what
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systole, which causes a contraction which gives a pulse
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what happens in the action potential
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2 sodiums are pushed out and 1 potassium is brought in so the outside has a positive charge and the inside is relatively more negative.
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what is depolarization caused by
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an advancing wave of positive ions
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what does depolarization of the heart cause
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the opeing of channels and entry of calcium from the t-tubles. this influx of calcium causes the calcium induced calcium release from the sarcoplasmic reticulum
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what does an increase in myoplasmic free calcium ions concentration lead to
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muscle contraction.
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where are the different ions when the heart is in a polarized state
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there is a high concentration of sodium and low concentration of potassium outside the cell. There is a high concentration of potassium and a low concentration of sodium inside the cell.
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what is the cell in the polarized state
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negative
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what happens in depolarization
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inside of the cell becomes more positive than outside of the cell.
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what are the accessory muscles
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scalene-raises the first and second rib
sternoclomastoid-raises the clavicles |
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what are some causes of acute onset pulmonary issues
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pneumothorax, PE, bronchospasm, asthma, reactive airway disease, foreign body, toxic inhalation
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what are some causes of an acute onset cardiac
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MI, papillary muscle dysfunction or rupture, ventricular dysfunction, cardiogenic pulmonary edema
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what is ventilation
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mechanical movement of air to and from atmosphere and alveoli
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what is diffusion
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movement of gases from high pressure to low pressure
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what is perfusion
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flow of blood past alveoli
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what are two things that need to be looked at for adequate ventilation
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resistance of system and lung compliance
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what can lead to increased resistance of the system
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tongue, gum ball, asthma, vomit, edema, hemorrhage, tumor, mucous plug
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what can lead to decreased lung compliance
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PE, ARDS< pneumonia, decrease in surfactant
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what can increase lung compliance
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emphysema
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what is normal lung compliance
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100
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what is lung compliance in ARF
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less than 20
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compliance is usually used to guide what
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increases in PEEP.
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what are the factors that affect diffusion
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diffusion coefficient, surface area, distance to be traveled, partial pressure gradient
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what is the equation for the A-a gradient
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PAO2-Pa02
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what is a normal A-a gradient
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less than 10 or 20
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what does the V/Q ratio determine
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the adequacy of gas exchange in the lung. When alveolar ventilation matches pulmonary blood flow, CO2 is eliminated and the blood becomes fully saturated with oxygen
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what is the most common cause of hypoxia
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VQ mismatch
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what is the normal alveolar ventilation rate
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4L/minute
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what is the normal pulmonary vascular blood flow at
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5L/minute
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what is the normal VQ ratio
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0.8
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what happens when a disease throws off the VQ equation
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leads to hypoxemia/hypoxia which causes right to left intrapulmonic shunting
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what happens in right to left shunting
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blood from the right side of the heart goes to the left side without gas exchange
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what can affect the VQ ratio
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gravitational forces
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what happens if an intrapulmonary shunt is greater than 30%
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resultant hypoxemia does not improve with supplemental oxygenation
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how do you estimate an A-a gradient
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age + 10/4
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what does a 10% increase in FiO2 lead to
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A-a increases 5-7 mmHg
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what causes an increase of an A-a gradient
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VQ mismatch or shunting
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what is the difference between sats and ABGs
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oxygen dissolved in the plasma 3% is (ABGs) and Pa02
oxygen that is attached to the hemoglobin is sats |
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what happens when 02 sats are down to 85-90
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mild tissue hypoxia
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what happens when sats are 75-85
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severe tissue hypoxia
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what is the normal Pa02
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80-100
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what is a normal pH
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7.35
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what is a normal PaCO2
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35-45
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what is a normal HCO3
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22-26
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does CO2 rise or fall with respiratory acidosis
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increased
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what are the causes of respiratory acidosis
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COPD, decreased function of the respiratory center, decreased LOC, anesthesia, narcotics, paralytics, hypoventilation, respiratory muscle failure
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what are the manifestations of respiratory acidosis
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headache, fatigue, tremors, confusion, lethargy
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what are the changes seen in respiratory alkalosis
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PaCO2 decreased, pH increased, normal HCO3
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what are the causes of respiratory alkalosis
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hypoxia, pain, pulmonary emblous, pneumothorax, asthma
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what are the manifestations of respiratory alkalosis
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anxiety, fever, mechanical hyperventilation, atelectasis, lightheaded, paresthesias, cramps
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what do you seen in metabolic acidosis
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HCO3 decreased, pH decreased normal PaCO2
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what are the causes of metabolic acidosis
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DKA, renal failure, dehydration, sepsis, lactic acidosis, severe diarrhea, aggressive volume replacement
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what are the manifestations of metabolic acidosis
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kussmaul breathing, ventricular arrhythmias, impaired neuro and or cardiac function, watch for hyperkalemia, and hyperchlremia
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how do you correct metabolic acidosis
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excrete excess acid and treat underlying cause
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how is metabolic acidosis compensated
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hyperventilation
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what do you see in metabolic alkalosis
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HCO3 increased, pH increased PaCO2 normal
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what are the causes of metabolic alkalosis
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NG drainage, diuretic therapy, aldosterone, vomiting, steroid therapy, excess HCO3 adminsitration
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what are the symptoms of metabolic alkalosis
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impaired cardiac function, symptoms of underlying disease, arrhythmias, neuro irritability, hypokalemia
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how do you correct metabolic alkalosis
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excrete HCO3, fix acid loss, restore fluids and lytes
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what are the manifestations of respiratory alkalosis
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anxiety, fever, mechanical hyperventilation, atelectasis, lightheaded, paresthesias, cramps
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what do you seen in metabolic acidosis
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HCO3 decreased, pH decreased normal PaCO2
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what are the causes of metabolic acidosis
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DKA, renal failure, dehydration, sepsis, lactic acidosis, severe diarrhea, aggressive volume replacement
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what are the manifestations of metabolic acidosis
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kussmaul breathing, ventricular arrhythmias, impaired neuro and or cardiac function, watch for hyperkalemia, and hyperchlremia
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how do you correct metabolic acidosis
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excrete excess acid and treat underlying cause
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how is metabolic acidosis compensated
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hyperventilation
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what do you see in metabolic alkalosis
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HCO3 increased, pH increased PaCO2 normal
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what are the causes of metabolic alkalosis
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NG drainage, diuretic therapy, aldosterone, vomiting, steroid therapy, excess HCO3 adminsitration
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what are the symptoms of metabolic alkalosis
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impaired cardiac function, symptoms of underlying disease, arrhythmias, neuro irritability, hypokalemia
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how do you correct metabolic alkalosis
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excrete HCO3, fix acid loss, restore fluids and lytes
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what is the compensation for metabolic alkalosis
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hypoventilate
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where are the lead 1 placements
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right arm-negative
left arm-positive |
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where are the lead II placements
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right arm-negative
left leg- positive |
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where are the placements for lead III
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left arm-negative
left leg-positive |
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what are the indications to put a patient on mechanical ventilation
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apnea, hypoxemia, respiratory acidosis, atelectasis, anethesthesia, decrease myocardial consumption, decrease ICP, stabilize chest
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what are the four objectives of mechanical ventilation
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adjust alveolar ventilation, maintain arterial oxygenation
increase lung volume reduce te work of breathing |
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what is total lung capacity
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volume in lungs after maximum inspiration
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what is tidal volume
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amount of air in and out normally. vents adjust this
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what is residual volume
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air left in the lungs after a maximal exhalation. Air that is always in the lungs and can never be expired
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what is functional residual capacity
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amount of the air left in the lungs after a normal tidal breath out
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what is a pressured cycled ventilator
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ventilator will deliver gas until the preset intra-airway pressure limit is reached...then it allows for expiration
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how do volume cycled ventilators work
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deliver gas until preset tidal volume is reached
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what are the consequences of a volume cycled ventilator
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damage caused by high intra airway pressure
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what are the types of modes in positive pressure ventilators
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controlled, assist/control ventilation, intermittent mandatory ventilation, synchronized intermittent mandatory ventilation, pressure support, high frequency, inverse ratio
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what happens in a controlled ventilator
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breaths are delivered at preset rate. No gas available for spontaneous breathing between preset breaths
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what happens in assist/control ventilation
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gas is delivered at a preset rate and tidal volume. Spontaneous ventilator effort triggers another breath of the preset tidal volume
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what is the risk in A/C
|
hyperventilation
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what is intermittent mandatory ventilation
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breaths delivered at preset rate and volume based upon time trigger
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what is synchronized intermittent mandatory ventilation
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breaths delivered at preset rate and volume based upon time trigger. Preset breaths are synchronized with patients own inspiratory effort.
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what does positive pressure ventilation do to CO
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increases intrathoracic pressure and reduces venous return. Drops right side preload
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what happens in inverse ratio ventilation
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inspiration is made to last longer than expiration. Keeps alveoli open, decreases sheer.
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what does pressure support ventilation do
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It supports or augments patient’s inspiratory effort …In response to the patients spontaneous inspiratory effort, the ventilator is triggered to deliver a high flow of gas to the patient until a preset intra-airway pressure is met.
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when is high frequency ventilation used
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when patient is hemodynamically unstable that a fall in CO would kill them so normal positive pressure can't be used.
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what is positive end expiratory pressure
|
intra-airway pressure maintained above baseline during all phases of ventilation
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what is the purpose of PEEP
|
to increase functional residual capacity
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what is the result of using PEEP
|
increased gas exchange surface area and increased PaO2
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what is continuous positive airway pressure
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the maintenance of airway pressure continuous above baseline when associated with spontaneous breathing
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what are the advantages of PEEP or CPAP
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lower FIO2, less shunting, increased compliance
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what are the disadvantages of PEEP or CPAP
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increase intrathoracic pressure- decrease in BP and CO, increase in PAWP and ICP, increase in atrial natruetic peptide which decreases urine output
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how do you control PaCO2 of pt. on ventilator
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adjust tidal volume and rate
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when is an increase in work of breath significant seen
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when tidal volume is less than 7mL/kg
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what are the recommendations to prevent VAP
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HOB up, wake up and wean them off, prophylactic stress ulcer prevention, DVT prevention, mouth care-use chlorhexidine spray/swabs
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what should you set the RR for a/c
|
12-16
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what should you set the tidal volume at for a/c
|
10ml/kg max
want 6-8 |
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what do you set I to E at
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1:2 or 1:1.5
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what is the flow rate
|
the speed that the tidal volume is delivered at
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what is the peak flow set at
|
50ml/min
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what should peak inspiration pressure be set at
|
less than 40
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what should inspiratory sensitivity be set at
|
-1
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how would you increase alveolar ventilation
|
increase rate or increase tidal volume
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how do you increase oxygenation
|
increase FiO2 or increase PEEP, or increase tidal volume
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what is used for pain control in ventilator patients
|
opioids
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what causes a low pressure alarm
|
leak, cuff tubing vent disconnect
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what causes high pressure alarms
|
kink secretions, biting, gagging, bronchospasm, pneumo
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what causes an increasing capnographic baseline (a-b)
|
rebreathing CO2
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what causes a disturbed downstroke on a capnogram
|
circuit leak
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what causes a rounded waveform on capnogram
|
kinked endotraceal tube or expiratory resistance
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what od you see if there is a kink
|
poor expiration
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what does end tidal CO2 estimate
|
pulmonary dead space, confirms placement of endotube, checks integrity of vent equipment
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what are the types of ACS
|
AMI and unstable angina
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what is significant ST segment elevation or depression
|
1mm above or 0.5mm below
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what does ST segment elevation on depression signify
|
injury
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what does T wave inversion signify
|
ischemia
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what signifies myocardial ischemia
|
t wave inversion, ST-segment depression
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what signifies myocardial injury
|
ST-segment elevation
T wave inversion |
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what signifies myocardial infarction
|
Q waves, ST segment elevation, T wave inversion
|
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what are the indications for vasoactive drugs
|
hypotension-CHF, acute MI, shock, cardiac arrest
hypertension-primary, secondary, hypertensive urgerncies, hypertensive crisis (MAP > 150) hypertensive emergency |
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how do vasoactive drugs treat hypotension
|
alter blood pressure and blood flow, improve cardiac function, maintain cardiac output, increase or decrease peripheral vasacular tone, increase HR and contractility
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how do vasoactive drugs treat hypertension
|
vasodilation, decrease afterload
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what are the types of vasoactive agents
|
arterial dilator, venous dilator, vasopressor
|
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how do vasoactive medications work
|
work through the sympathetic nervous system
|
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what are the three receptors of the sympathetic nervous system
|
alpha adrenergic, beta adrenergic, dopaminergic
|
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what do catecholamines do
|
speed up the cardiac system
|
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what are the types of catecholamines
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epinephrine and norepinephrine
|
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what does epinephrine do
|
increases cardiac output
increases depth of breathing pounding heart feeling |
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what does norephinephrine do
|
vascular constriction, increased blood pressure, dilated pupils
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where are the alpha receptors primarily located
|
in arteriols
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what do alpha receptors effect
|
vasoconstriction-increase SVR, afterload and BP
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what are beta 1 receptors located
|
myocardial cells, sinoatrial node, AV junction
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what is the effect of beta-1 receptors when stimulated
|
increase heart rate, increase contractility, increase in AV conduction
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what happens when beta 1 receptors are blocked
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decrease in HR, decrease in contractility, decrease in CO, decrease in BP, slow av node conduction
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where are beta-2 receptors located
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lungs and peripheral vasculature
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what is the effect of beta-2 receptors when stimulated
|
bronchodilator, vasodilator
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what is the effects when beta-2 receptors are blocked
|
blood vessels constrict, lungs constrict
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where are dopaminergic receptors located
|
renal and mesenteric vessels
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what happens when dopaminergic receptors are stimulated
|
increase blood flow to kidneys
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what are the chronotropic influences
|
incluences the heart rate
|
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what does a positive chronotropic influence do
|
increases heart rate
|
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what does a negative chronotropic agent do
|
decreases the automaticity of the SA node, slows the heart rate
|
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what do inotropic agents influence
|
myocardial contractility
|
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what does a positive inotropic agent do
|
increases contractility, increases stroke volume
|
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what is the action of dopamine
|
precursor of norephinephrine. direct activation of specific dopaminergic receptors in the mesenteric and renal vasculature resulting in vasodilation and increased renal blood flow
|
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what does low dose dopamine do
|
dopaminergic effect or beta effect: dilates bronchiole, increases renal flow, increases urine output, little or no effect on BP
|
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what is the effect of middle dose dopamine
|
some renal perfusion effects, increased blood pressure, increased heart rate, increased cardiac output
mostly beta 1 and some alpha effect |
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what does high dose dopamine do
|
pure alpha effect-vasoconstriction, increased cardiac output, increased heart rate, decreased urine output, decreased renal perfusion
|
|
what are the side effects of dopamine
|
hypertension, necrosis of tissue at IV site, tachycardias, tachyarrhythmias
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what are the nursing implications for dopaine
|
monitor BP q 15 minutes once BP is stabilized. Acidosis decreases effectiveness of dopamine. Regitine is antidote for extravasation of dopamine into tissue
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what is the action of dobutamine
|
directly stimulations beta 1 receptors of the heart to increase contractility and stroke volume with only a mild increase in HR and BP
|