Archer: Critical Care Concepts

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46 Terms

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Ventilators terminology

continue to next following flashcards

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peak inspiratory pressure (PIP)

highest level of pressure in lungs during inhalation

(pressure going in)

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positive end expiratory pressure (PEEP)

amount of pressure in the alveoli at the end of expiration

(pressure at the end)

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fraction of inspired oxygen (FiO2)

how much oxygen the patient is getting (21%-100%)

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tidal volume (TV)

the amount of air that is inhaled during one respiratory cycle

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end-tidal carbon dioxide (ETCO2)

partial pressure of CO2 at the end of exhalation (35-45)

if it is low then retaining CO2 thus making them acidotic

if it is high then releasing CO2 thus making them alkalotic

CO2 is acid

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room air

atmospheric air we breathe under normal circumstances. has FiO2 of 21%

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Ventilator modes

-volume controller: there is certain volume of air delivered to the pt. with each breath

-pressure controlled: the lungs are inflated to a certain pressure (looks at PIP and PEEP)

-CPAP: continuous positive airway pressure; continuous positive airway pressure, occurring, while pt controls their respiratory rates and volumes

-BiPAP: bilevel positive airway pressure; there is positive airway pressure, set at diff pressures for inspiration and expiration

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high pressure alarms are activated by

pressure in the circuit that is too high

-anything that blocks, kinks, occludes, pushes

causes:

-pt. coughing

-gagging

-bronchospasm

-fighting the ventilator

-ETT occlusion

-kink in tubing (clogged)

-increased secretions

-thick secretions

-water in ventilator circuit

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low pressure alarms

pressure in circuit is too low

-leaklike, disconnection, something came apart

causes:

-tubing is disconnected

-loose connections

-leak

-extubation

-cuffed ETT or trach is deflated

-poorly fitted CPAP or BiPAP mask

-pt. pulls out tube

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Hemodynamic monitoring

terminology for hemodynamic monitoring; continue in following cards

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preload

amount of blood returning to right side of the heart (deoxygenated blood from body coming back)

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afterload

pressure against which the left ventricle must pump to eject blood out to body

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compliance

how easily the heart muscle expands when filled w blood

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contractility

strength of contraction of the heart muscle

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stroke volume

volume of blood pumped out of each ventricles with each contraction (measured in a percentage)

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cardiac output

amount of blood pumped out by cardiac system every MINUTE

formula is for CO is SV x HR

<p>amount of blood pumped out by cardiac system every MINUTE</p><p>formula is for CO is SV x HR</p>
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why cardiac output so important?

-tissue perfusion

-delivery of oxygen and nutrients to each and every cell in body

-for organ function

poor cardiac output?

-brain: decr. LOC

-heart: chest pain, weak peripheral pulses

-lungs: SOB, crackles, rales

-skin: cool, clammy, mottled extremities

-kidneys: decr. UOP

CO = Stroke volume x heart rate

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incr in preload leads to what with CO?

incr in CO (more blood coming back to heart then more blood coming out per min)

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incr. in afterload leads to what with CO?

decr. in CO (incr in afterload makes increase in pressure so more difficulty pumping blood w heart, so decr CO)

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incr in compliance leads to what in CO?

incr. CO (more expansion)

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incr in contractility leads to what in CO?

incr CO (the muscle can contract stronger to pump out blood incr CO)

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incr. in stroke volume leads to what in CO?

incr. CO (more blood pumped with each contraction means more blood pumped per min)

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causes of dec. CO

-bradycardia (slow HR)

-arrhythmias (pulseless V-tach, V fib, asystole, supraventricular tachycardia)

-hypotension

-myocardial infarction

-cardiac muscle disease

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causes of incr. CO

-incr blood volume

-tachycardia

-medications (ace inhibitors = cause vasodilation and decr. afterload, ARBs = decr afterload, nitrates = decr afterload)

-inotropes = incr. contractility

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cardiac output

4-8 L/min

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cardiac index

2.5-4.0 L/min/M^2

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when do you need vasoactive infusions

-cardiac arrest

-hypotension

-shock refractory to fluid resuscitation

-cardiac disease (acquired or congenital)

-decr. cardiac output

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Inotropes:

act on force of myocardial contractility (incr. contractility)

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vasopressors

mimic sympathetic nervous system to cause vasoconstriction = squeeze veins to incr. BP

-for pt w low BP

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adrenergic receptors

receptor sites that sit in vascular smooth muscle, heart, all thru body monitoring to create diff reactions based on what occurs

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alpha 1 receptor

found in vascular smooth muscle

-veins

-monitor BP

-when BP goes down = causes vasoconstriction to incr BP

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beta 1 receptor

in heart

-monitor BP

-when it goes down it incr. contractility

-incr. SV, HR, and CO

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beta 2 receptor

in lungs

-how well dilated the bronchi and vasculature leading to lungs are ok

-are lungs getting enough blood

-causes bronchodilation

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epinephrine

-most often used in cold shock

-low doses act on beta 1 receptors: incr contractility, thus incr. CO

-high doses act on alpha 1 receptors: incr. vasoconstriction, incr. BP

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norepinephrine

-most often used in warm shock

-acts on alpha 1 receptors: incr. vasoconstriction, thus increasing BP

-incr. cardiac output

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dopamine

-used in trauma pt. and cold shock

-low doses used in kidney failure to incr. renal blood flow (renal dopa) :: low doses incr. contractility => incr. CO

-higher doses cause vasoconstriction => incr. SVR => incr. BP

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phenylephrine

-used for anesthesia-induced hypotension

-second line agent in some shock pt.

-only acts on alpha 1 : incr. vasoconstriction thus leading to incr. BP

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milrinone

used in pt. with cardiogenic shock, decr. cardiac output, congenital/acquired heart defects

-causes systemic vasodilation, pulmonary vasodilation, decr. afterload, incr. contractility

-doesnt incr. oxygen consumption

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vasopressin

-antidiuretics hormone (ADH)

-less diuresis => hold onto water => more volume thus more pressure => raises BP

-second line in vasodilatory shock

-third line in septic shock

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complications and side effects of vasoactive infusions

-arrhythmia: due to stim. of beta 1 receptors

-hypoperfusion to extremities, kidneys, and GI tract: due to excessive vasoconstriction

-peripheral tissue necrosis: due to hypoperfusion of the skin

-myocardial ischemia (obstructed blood flow to heart): due to incr. myocardial oxygen demand secondary to incr. chronotropy

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unconscious pt.

1. try to wake pt, yell and shake them & sternal rub

2. check their pulse (adult: carotid) (infant: brachial) - for no longer than 10 sec.

3. press the code bell and yell for help

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priority intervention if they have no pulse

-start chest compressions (100-120 bpm); depth of 2 inches, allow full chest recoil

-have someone get crash cart

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CPR cycles

-30 compressions: 2 breaths

-2 minutes

-at 2 min mark: check rhythm and pulse

-if pt. still pulseless, switch compressors and resume compressing

-never stop compressions for more than 10 secs.

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shock

-allow AED to analyze rhythm

-follow prompts

-if shock advised, resume compression while device charge

-clear pt. when AED advises

-ensure pt is cleared and administer shock

-immediately resume compressions

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infant CPR

2 rescuer: compression to breath ratio is 15:2

1 rescuer: 30:2

use 2 fingers for compression

-compress a depth 1/3 of chest to back diameter