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115 Cards in this Set
- Front
- Back
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surfactant:
inc/dec surface tension? |
decreases
decreased surface tension=increased lung compliance making it easier for lungs to inflate |
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how does surfactant aid in preventing pulm edema?
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keeps alveoli dry
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Dx notorious for decreasing surfactant prod
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ARDS
Dec surfactant=inc surfacae tension and dec lung compliance making it harder for lungs to inflate |
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Dx's that can decrease lung compliance
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COPD (fibrosis), ARDS (via dec surfactant)
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What role does slight negative intrapleural pressure serve
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Helps keep alveoli open
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What might increase airway resistance
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Pulmonary secretions, bronchospasms.
Small changes in diameter can lead to enormous changes in flow (ventilation) and thus inc WOB |
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fx of hypervent on PaCO2
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decreases PaCO2 (alkalotic)
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fx of hypovent on PaCO2
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increases PaCO2 (acidosis)
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term for air w/in conducting airways that ultimately does not reach alveoli
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anatomical dead space (often assoc w/ COPD)
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Intervention for decreasing anatomical dead space
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dependant upon body position****
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Terminolgy when perfusion is decreased/absent but ventilation is normal
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Physiological/alveolar dead space
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AKA for physiological dead space
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Alveolar dead space i.e. decreased/absent perfusion
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physiological dead space AKA alveolar dead space refers to
1) decreased/absent perfusion 2) decreased ventilation |
1) decreased/absent perfusion
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Som factors that may thicken capillary membrane and fx diffusion of gasses
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secretions, intersitial lung Dx, pulm edema
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Best overall body position for VQ matching
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Semi folwers
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physiologic shunt. Problem with
1)bf 2)alveoli |
alveoli
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Physiologic shunt.
1) high VQ (vent>perfusion) 2) low VQ (perfusion>vent) |
Low VQ
Problem with ventilation/alveoli so, Perfusion>ventilation Blood is passing by alveoli wihtout gas exchange |
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Term for VQ imbalance when adeq bf is passing by alveoli but gas exchange is not occuring
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Physiologic Shunt
Problem with Alveoli Low VQ (perrfusion>vent) |
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Cndx's causing physiologic shunt
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Think about condz's reducing ventilation
Pneumonia Atelectasis Mucus plug |
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Alveolar/physiologic dead space. Problem with
1) bf 2) alveoli |
Blood flow
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Alveolar/physiologic dead space.
1) High VQ (vent>perfusion) 2) Low VQ (perfusion>vent) |
High VQ
problem with bf so, High VQ (ventil>perfusion) |
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term for VQ imbalance when blood flow to alveoli is reduced and gas exchange can not occur
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Alveolar/physiologic dead space
problem with b.f. High VQ (ventil>perfusion) |
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Condx's causing alveolar dead space
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PE r/t blockage
Cardiogenic shock (dec CO and thus poor lung perfusion) Pulm HTN Mechanical vent (increases intrathoracic pressure) |
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Silent unit. Problem with
1) bf 2) alveoli |
Both
Dec in both vent and perfusion |
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Cndx's causing silent unit
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Pneumothorax
ARDS |
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represents amt of O2 dissolved in plasma
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PaO2
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Normal PaO2
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80-100
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Normal SaO2
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93 or greater
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represents the amt of hemoglobin molecules bound with O2
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SaO2
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Most O2 supplied to tissues as PaCO2 or SaO2
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SaO2
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PaO2<?? = large changes in SaO2
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60
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More negative fx for pt
1) High affinity of O2 for Hb 2) Low affinity of O2 for Hb |
High affinity
At tissue level tight bond does not readily release O2 |
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stims inspir/expir of diaphragm and itnercostals
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medulla
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controls apneustic center and pneumotaxic center
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pons
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chemoreceptros in periphery stim increased respirs when PaO2<??
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60
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Causes decreased SvO2
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May indic
1)decreased o2 supply -dec H&H -Dec CO -dec arterial sat 2) increased O2 usage -fever -stress -anxiety -pain |
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Resp acidosis caused by
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1) CNS depression r/t head inj, sedatives/analgesia/narcotics
2)Pulm d/o i.e. PE, COPD, pneumonia, pulmonary edema 3) Pain |
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Mgmt/Tx of resp acisdosis
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MV usually all thats required
Other measures -Pain mgmt -Pulm toilet |
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What is done in pulmonary toilet
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-Increase HOB
-Secretion removal -Cough/deep breath -Incentive spirometry |
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Causes resp alkalosis
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Panic attacks
Pain/fever/sepsis |
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Causes tetany (hypoCa)
1) alkalosis 2) acidosis |
alkalosis
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Mgmt/Tx resp alkalosis
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Ativan if anxiety d/o
Paper bag/rebreather Pain mgmt |
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Causes of increased acids in metab acidosis
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Renal failure-
Ketoacidosis Anerobic metab>inc lactic acid secondary to lack of O2 to tissues Salicylate toxicity |
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Causes of loss of base in metab acidosis
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Diarrhea
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Kussmaul's respirs assoc with what acid/base d/o
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Metab acidosis/DM/ketoacidosis
Compens mech to try and blow off acid/CO2 |
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Mgmt/Tx metab acidosis
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Treat underlying d/o (ketoacidosis, renal failure, hypoxia/anerobic metab)
AND IV sodium bicarb |
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IV sodium bicarb indic in what acid/base d/o
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Metab acidosis
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Diamox indic in what acid/base d/o
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Metab alkalosis
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Which acid/base d/o most requires cardiac monitoring
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Metab acidosis-lots of arrhythmias
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What may cause loss of acids in metab alkalosis
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Excessive vomiting/NG suction
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What might lead to gain of base in metab alkalosis
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Excess bicarb in codes
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Mgmt/Tx metab alkalosis
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Diamox
Tx underlying cause -excess: bicarb, suction, diuretics |
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O2 flow with nasal cannula
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1-6
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O2 flow with simple face mask
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6-8
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O2 flow with non-rebreather
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12-15 (although still technically not 100%)
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example of high flow O2 delivery system
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venturi
-Most reliable and accurate method for precise concentrations of O2 -Constant O2 is inhaled despite pt’s RR and depth of respires |
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O2 toxicity a concern when FiO2 is > ?? for ?? long
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>50
>48h Goal is to titrate to lowest setting while maintaining PaO2>60 or SpO2>92 |
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O2 toxicity carries risk of
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Alveolar capillary leakage leading to pulmonary edema
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Measures to prevent vomit/aspiration druing ETT placement
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Suction and sedation
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Why is it impt to monitor for SpO2, HR and BP during ETT placement
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Arrhythmia (hypoxemia)
Cardiac arrest |
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Measures to ck placement of ETT
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Auscultate (evaluate for R main stem intubation-would only hear l.s. on one side)
CXR (203 cm above carine) |
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indications for suctioning
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-Dec SaO2
-Vent alarms -Coughing -Auscultation -Visual observance of secretions |
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Acute resp failure
PaO2<?? PaCO2>?? |
PaO2<50
PaCO2>50 pH<7.35 Resp acidosis with hypoxemia |
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Causes of hypoxemic resp failure
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V/Q mismatch-Physiologic shunt (not a prob with blood flow)
Partially collapsed alveoli, alveoli filled with fluid Pnemonia, atelectasis, mucus plug |
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This diagnostic study assists in confirming type (I, II, III) of acute resp failure
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ABG
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1st line Tx to correct resp acidosis in acute resp failure
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Increase alveolar ventilation and pulm toilet
MV-blow off O2 Tx underlying Dx process (pneumothorax, head injury) |
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Nute support in acute resp failure pt
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Enteral
Little carbs |
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Why are carbs not increased in enteral feeds with acute resp failure/ARDS
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Carbs increase CO2 production
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3 criteria for Dx of ARDS
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-Hypoxia refractory to FiO2 admin
-Non-cardiogenic pulm edema-PAWP <18 (>18 would indic HF) -CXR consistent with bilat infiltrate AKA white out |
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Examples of direct pulmonary injury in ARDS
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Aspiration of gastric contents
Pulmonary infection |
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Example of indirect pulmonary injury in ARDS
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-Shock/Sepsis-Big risk, majority end up in ARDS
-Hypo/hyper-htermia -Pancreatitis -Burns/Trauma |
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Type of V/Q mismatch in ARDS
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Silent unit
1)Intrapulm shunt -Alveolar/capillary membrane damage>alveolar edema -Dysfxnal surfactant>alveoli not open/dry -mediator induced bronchoconstriction 2) Alveolar dead space (decreased lung perfusion) -Pulm HTN |
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Stage 1 (1st 12 hours)manifestations of ARDS
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Hardly any
1) Increased SOB and RR mimics many other Dx processes 2) CXR normal showing no cellular damage |
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Stage at which CXR begins to show patchy infiltrates in ARDS
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2-withing 24 hours of onset
Also refractory to O2 requiring MV |
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Stage at which ARDS becomes resistant to O2 admin and requires mechanical vent
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2-within 24 hours
Also CXR begins to show patchy infiltrates |
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ARDS stage at which you begin to see hemodynamic instability
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3-2-10 days
FiO2 req continues to increase as well as need for PEEP White shows on CXR |
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Stage at which white shows on CXR in ARDS
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3-2-10 days
Hemodynamic instability seen FiO2 req continues to increase as well as need for PEEP |
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Early ABG's in ARDS
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Resp alkalosis
Resp acidosis dvp's as ventilation worsens and continues to get worse despite interventions |
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PaO2 in ARDS
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<6o and gets worse despite increasing FiO2
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In ARDS transfuse when Hb<??
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8
Improves O2 delivery |
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Controversial method of improving CO in ARDS
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Fluid administration b/c of SIRS mediated vasodil
BUT Potential for 3rd spacing d/t SIRS endothelial changes Get Swann |
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Pharmacological means of increasing CO in ARDS
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Inotropes-dopa, dobuta
Pressors-dopa (high dose, norepi, levophed |
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MV settings in ARDS
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-Probably FiO2 of 100% (would like to titrate down if possible but usually not possible)
-Small tidal volume to account for still lungs -PEEP 10-15 |
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Term for prone+kinetic
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Rotoprone
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rotation<40 degrees
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Continuous lateral rotation
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rotation>40 degrees
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Kinetic
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Benefits of prone positioning in ARDS
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-Pulls perfusion to anterior portion of lungs thereby increasing oxygenation
-CXR resolution |
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Rx for ARDS
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None specific
-Steroids-decrease inflammation in lung and intravasc tissue -Bronchodilators/mucolytics -Abx for VAD prophylaxis |
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Etiology of protein wasting in ARDS
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1) SIRS allows for protein wasting via capillary leakage
2) Mediators release proteolytic enzymes which stim catabloism -Promot nute therapy essential |
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# of kcal/kg/day in ARDS
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35-45
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2 pt populations at great risk for PE
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Post surg (specifically hip/knee)
ICU pt's in general d/t immobility |
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Virchows triad
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1) Venous stasis>clots
2) Hypercoagulabilty-immobiliz secondary to surgery 3) Endothelial changes e.g. incisions |
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Majority of PE/DVT arise from?
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popliteal/ileofemoral
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Type of V/Q mismatch in PE
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Alveolar/physiological dead space i.e. problem with perfusion d/t occlusion of PA artery
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In PE hemodynamic changes occur when blockage>??
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30-40%
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In PE Hemodynamic changed b/c severe when blockage>??
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50%
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What hemodynamic parameters change in PE
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Increased
-CVP -PAP Decreased -CO -BP |
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Normal PAP
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20-30/8-15 (20-30)
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Normal CVP
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<8
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Normal PAWP
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8-12
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S&S of DVT
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pain
Edema/swelling redness Does not affect pulses S&S absent in 25% |
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Most common manifestations of PE
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SOB and inc RR (very non-specific)
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Test of choice in PE with stable pt
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VQ scan
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Test of choice in unstable pt
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Pulm angiography
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Gold standard for Dx in PE
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Pulm angiography
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Nursing interventions/monitoring for Pulmonary angiography
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BUN/Creat r/t die
Bleeding |
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Emergent mgmt of PE
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O2
Establish airway/IV Maintain CO Prepare diagnostic test |
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When are thrombolytics indic in PE
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massive PE/hemodynamically unstable
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C/I to thrombolytics in PE
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cranial bleed
recent surgery (which may be highly likely) |
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Nursing interventions/monitoring for thrombolytics in PE
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PT/PTT/INR/H&H
Get foley, NG/DT, IV's in before initiation Watch for bleed Monitor vitals |
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PTT goal with heparin in PE
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1.5-2.5 X normal
45-70 sec |
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Indication for IVC filter
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Chronic/recurrent PE/DVT
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S&S of IVC filter clotting
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Increasing LE edema
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In ARDS, what causes decreased lung compliance
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Surfactanct production inhibited>surface tension increases>lungs become harder to inflate
Ventilatory capacity is decreased |
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PAWP must be < ?? for ARDS to be Dx'd
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18 i.e. non cardiogenic pulm edema
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