cdunbar4's version from 2017-03-31 02:35

Assessment/Clinical Findings (from narrative)

Question Answer
Definition Acute Respiratory Distress syndrome (ARDS)sudden and progressive form of acute respiratory failure in which the alveolar-capillary interface becomes damaged and more permeable to intravascular fluid
Most common causesepsis
Other two causesDirect lung injury/SIRS
ARDS is a clinical syndrome, NOT a single-organ diseasedescribes the pulmonary manifestation of alveolar damage that occurs with many different disease processes
Initial clinical manifestations of patient with ARDSdyspnea, tachypnea, cough, and restlessness
What will ABGs show?mild hypoxemia & respiratory alkalosis (caused by hyperventilation)
What will a chest x-ray reveal?could be normal or could show minimal scattered interstitial infiltrates
Edema may not show up initially on xray until what happens?until their is an increase in fluid content in the lungs (about 30% of an increase)
As ARDS progresses, what causes ↑ WOB, tachypnea & retractions to occur?increased fluid accumulation & decreased lung compliance
Collaborative treatment of patient who has severe progression of ARDSendotracheal intubation
What does chest xray show at later progression stages?whiteout as consolidation & infiltrates are widespread throughout lungs

Collaborative Care (from narrative)

Question Answer
Complications of ARDSventilator assisted pneumonia; barotrauma; stress ulcers & renal failure
Patient with ARDS needs what type of supportive therapies?oxygen administration, positive pressure ventilation, and medical supportive therapy
O2 therapy helps to correct hypoxemia by keeping the PaO2 >? 60mmHg (intubation & mechanical ventilation)
Positive pressure ventilation (PEEP) helps the lungs do what?keeps alveoli open
If pt. remains hypoxic, even with PEEP, what else can be used?extracorporeal membrane oxygenation (ECMO)
How does ECMO work?passes blood across a gas exchanging membrane outside the body and then returns oxygenated blood to the body which allows the lungs to heal while they're not being used
Patient positioning, supine or prone?Prone. Turning from supine to prone will turn the nonatelectic, air-filled alveoli into the dependent areas which could help match perfusion to ventilation.
Supine positionheart and mediastinal contents put more pressure on lungs
What device can be used to help V/Q in relation to patient positioning?placing patient in continuous rotation beds that turn slowly side to side
Goals of treatment of ARDSmaintain CO & tissue perfusion
What type of monitoring will these patients need in order to monitor perfusion?hemodynamic monitoring, BP monitoring by arterial catheter (also allows for ABG blood draws)
IV infusion of what two drugs may be necessary?dobutamine or dopamine (inotropic agents to ↑ ability of heart to get blood circulated)
Other goals of treatmentmaintenance of nutrition & fluid balance → dietary consult will be needed to determine optimal caloric needs
Type of feedings that may be needed to meet high-energy requirements of these patientsenteral or parenteral feedings
Monitoringhemodynamic parameters, daily weights, intake and output to assessed the patient's fluid status.
PEEP Goal with ARDSadminister oxygen at the lowest possible level to support tissue oxygenation and avoid oxygen toxicity; keep alveoli open

Respiratory Failure (from ppt)

Question Answer
Acute respiratory failurea syndrome that presents as a rapidly occurring inability of the lungs to maintain adequate oxygenation of the blood (w. or w.o. CO2 elimination impairment).
Two types of acute resp. failurehypoxemic (aka Type I) or hypercapnic (aka Type II) *can be both!
Progression to ARDSis seen as a worsening on a continuum of lung/alveolar functioning...ARF→ALI→ARDS
Onsetcould be over minutes or days
Most common cause of arterial hypoxemiaV/Q mismatch
Most causes of hypercapniareduced minute volume, increased dead space/Vt ratio, usually due to rapid shallow breathing.
Mortalitygenerally depends on other comorbidities such as COPD, DM or other chronic illnesses/general health
Difference b/t ARDS and ARFARDS is acute characterized by widespread inflammation of lungs whereas ARF can be acute or chronic and is characterized by inadequate gas exchange by the respiratory system.
Criteria for ARF: PaO2 level<60mmHg with pt. at rest and on room air
Criteria for ARF: PaCO2 level>50mmHg with pt. at rest and on room air
Criteria includes AcidemiapH less than 7.30
SaO2 in ARF88% or less

When failure progresses to Acute Lung Injury (ppt.)

Question Answer
The criteria to diagnose ALI includesBilateral pulmonary infiltrates; Severe hypoxemia without cardiogenic pulmonary edema; Decreased lung compliance; Capillary leaking is exhibited clinically as non-cardiogenic pulmonary edema; PAWP less than 18 mmHg
Progression of ALI to ARDS is determined byPaO2/FiO2 ratio
PaO2/FiO2 ratio refers tothe patient’s ability to achieve and maintain oxygen saturation while receiving supplemental oxygen (regardless of the amount of positive end expiratory pressure [PEEP], if it is being used).
In order for calculation of PaO2/FiO2 to work, what must O2 administration (FiO2) be at? What other lab do you need (where do you get the PaO2 from)?45%; Patient PaO2 is from the ABGs
Healthy lung PaO2/FiO2 ratioexceeds 400
ALI PaO2/FiO2 ratioless than or = 300
PaO2/FiO2 ratio when ALI progresses to ARDS< or = 200

ARDS (from ppt)

Question Answer
Direct vs. indirectinjury to lung epithelium vs. insult to area outside of lungs & mediators travel to lungs via bloodstream
Indirect causes of ARDSsepsis; multiple trauma; DIC; massive transfusions; drug od; burns; fat emboli; anaphylaxis
Direct causes of ARDSaspiration of gastric contents; inhalation injury; O2 toxicity; pulmonary contusion; chest trauma; pneumonia (viral/bacterial); acute hemorrhagic pancreatitis; near-drowning
3 phases of pathophysiology of ARDSAcute Exudative, Proliferative and Fibrotic
Acute Exudative phaseInitial insult to pulmonary system → inflammatory mediators are release →massive production of neutrophils, macrophages & plts in pulmonary capillaries → leaks into alveoli flooding them with a protein-based exudate & inflammatory cells → interstitial edema/alveolar flooding = ↓ surfectant = alveolar collapse = hypoxemia=↓compliance & ↑ WOB

Physiologic consequences of ARDS & PFTS

Question Answer
Refractory hypoxemiaPaO2/FiO2 ratio <200
A-a gradientalveolar O2 minus arterial O2: PAO2 = pressure of oxygen in alveolus/O2 delivered to alveoli [whereas PaO2=pressure of oxygen in arterial blood (measured in ABGs)]
Increased A-a gradient(in other words the PaO2 is low despite a high FiO2 level trying to put O2 in).
Decreased lung compliancedecreased FRC (functional residual capacity) due to atelectasis and edema
Pulmonary HypertensionNormal PAOP (pulmonary artery occlusive pressure) with High PVR (pulmonary vascular resistance aka the opposition encountered by the right ventricle)
Increased dead space ventilationventilation WITHOUT perfusion (example: if a PE prevents blood flow through capillary)
Shuntinglarge R to L of 15-20% of CO on 100% O2
ABG resultsresp. alkalosis & hypoxemia (↓PaCO2 d/t tachypnea)
Clinical presentation of hypoxemiarestlessness; agitation; disorientation/confusion/delirium; dyspnea; arrhythmias; tachycardia; cyanosis; labored breathing; tachypnea
Clinical symptoms of hypercapniah/a; somnolence; coma; confusion
Clinical presentation of hypercapniaHTN; muscle twitching; diaphoresis; papilledema
Drugs for Sedationmay be continuous or with boluses of fentanyl, morphine, midazolam, lorazepam
Drugs for ParalysisPropofol, Precedex
Assess body systems during sedationfor tolerance & hemodynamic stability. Constantly monitor level of sedation!
Possible tools to monitor sedation levelMAAS (Motor Activity Assessment Scale); MSAT (Minnesota Sedation Assessment Tool); RASS (Richmond Agitation Sedation Scale); Riker SAS (Sedation-Agitation Scale)
Fluid Management (crystalloids or colloids preferred?)crystalloids such as LR or NS
ARDS can have serious consequences, monitor VS closely forworsening of pulmonary edema, ARDS can lead to MODS

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