W4 D2 - Respiratory issues Flashcards
pulmonary edema, emboli, pneumothorax, VAP, ARDS, pleural effusion
Classify pulmonary edema
Cardiogenic pulmonary edema
* left ventricular failure
* MI
* cardiomyopathy
* mitral/aortic valve stenosis
Non-cardiogenic pulmonary edema
* infection, sepsis
* pnemonia, aspiration
* multiple transfusions
Explain the patho for causes of pulmonary edema and classify
Pulmonary edema is a back up of fluid into the lungs
Stage 1 - dry interstitium. Fluid moves into interstitium, but lymphatic system removes it
Stage 2 - interstitial fluid. Lymphatic system is overworked
Stage 3 - fluid in alveoli. Fluid moves to alveoli and they may collapse
Cardiogenic pulmonary edema
Blood backs up into the lungs from a heart related issue
* left ventricular failure
* MI
* cardiomyopathy
* mitral/aortic valve stenosis
Non-cardiogenic pulmonary edema
Fluid/blood backs up into the lungs d/t a systemic issue
* infection, sepsis
* pnemonia, aspiration
* multiple transfusions, TRALI
*
Explain the patho of TRALI
Explain assessments, labs, test, & management of pulmonary edema
Assessment
Onset - gradual or sudden
Inspection - increase WOB, SOB, RR, JVD, tachy, ^BP
Auscultation - extra heart sounds, crackles
Results
* Chest xray
* echocardiogram
Managment
* BIPAP/CPAP
* ventilation/PEEP
* meds to decrease preload / hydrostatic pressure
* fluid restriction
Explain the patho of a PE
Massive PE = clot resulting in 50% occlusion in pulmonary circulation
Results in
* impaired gas exchange - bronchoconstriction
* cardiac dysfunction
Affected lung
* hypoxemia - VQ mismatch
Unaffected lung
* ^ perfusion
* v time to oxygenate
* ^ hypoxemia
Cardiac dysfunction
* RV ^ afterload - dysfunction
* pulmonary vasoconstriction
What are the types of emboli?
What are the classifications of PEs?
finish
Massive
* acute
Submassive
* acute stable
Low risk
* normal BP
* no evidence of MI
What are some risk factors for PE?
Virchows triad
* venous stasis - immobility, afib, prenancy, vLOC
* hypercoagulability - contraceptives, coagulation disorders, malignancy
* Vessel damage - trauma, surgery
Why would a patient develop right ventricular failure d/t PE?
Primarily because of the increase in afterload
* too tired to keep pushing against the resistance of smaller vessels
What assessments findings would you expect for a patient with PE?
- respiratory distress
- wheezes
- v air entry
- pleuritic chest pain
- respiratory alkalosis/acidosis
- tachycardia
- hypotension
- distended neck veins
- hemoptysis
- arrhythmias
- DVT signs
How do you diagnose a PE?
Spiral CT w/ contrast
V/Q scan to assess lung
Chest xray - atelectasis, dilated pulmonary vessels
Echo - assess RV
Doppler ultrasound - assess for DVT
ABG - respiratory alkalosis/acidosis, metabolic acidosis
What assessment findings will you see in pneumothorax?
Inspection/palpation
* decreased chest expansion
* respiratory distress
* tracheal shift
* asymmetrical chest expansion
* subcut emphysema
* respiratory distress
Auscultation
*
Mechanical ventilation
*
Differentiate open, closed, tension pneumothorax
Open
* laceration of chest wall and pleural cavity
* fractured ribs
Closed
* tear in visceral pleura
* high peep causing barotrauma
Tension
* air enters but cannot exit on expiration
* open or closed
* causes mediastinal shift, tracheal deviation
How would you manage a patient with PE?
Ventilation - mode, peep, FiO2
Hemodynamics - inotropes, fluids, BP support
Anticoagulants - IV heparin, LMWH
* prevention and thinning but not to break down
Thombolysis for massive PE - alteplase, risk of bleeding
Catheter directed treatment - thrombectomy
IVC filter
What is the treatment for pneumothorax?
Greater than 15% of lung requires treatment
Open/closed
* chest tube
Tension
* needle thoracentesis
* chest tube
Hemothorax
* chest tube
* blood products
What are some risk factors of VAP?
ETT / reintubation
* bypasses upper airway/no filter
* oral pathogens
* micro aspirations
* biofilm
Other
* lung disease
* smoking
* immunosuppressed
* sepsis
* decreased LOC
* aspiration
* immobility
* supine
* NG tubes
* histamine blockers
Explain the patho of VAP
- Pathogens enter alveoli
- Type 3 cells attack pathogen
- Damaged cells release cytokines that intitiate the inflammmatory process
- Cytokines vasodilate capillaries and increase permeability
- WBC migrate from capillary to alveoli
- Pathogens are destroyed
- Alveoli fill with exudate
- Results in ventilation perfusion mismatch
What assessment findings would you expect with VAP?
Inspection
* productive cough
* purulent sputum
* febrile
* vent alarms
Auscultation
* crackles
* decrease breath sounds
How do you diagnose VAP?
Chest X-ray
WBC more than 12000, less than 4000
Febrile
Secretions
Breath sounds
Worsening gas exchange
Sputum cultures
How do you prevent a VAP?
VAP bundle
* elevate HOB > 45 degrees
* daily sedation interruption
* spontaneous breathing trials
* use of subglottic ETT
* oral care
* oral gastric tube
* initiation enternal feeds
* mobility
* hand hygiene
What is ARDS?
**Non-cardiac pulmonary edema and disruption of capillary membrane **
* caused by injury to pulmonary vasculature and alveoli
* injury causes inflammatory response;
Explain ARDS phases
Exudative phase
*
Why is the lung compliance decreased iihth ARDS?
What causes hypoxemia in ARDS?
p
Destruction of type I cells leading to decreased oxygen diffusion
What are some key assessment findings in ARDS?
Explain the diagnosis of ARDS
Berlin definition 2012
* occurs within 1 week of known insult
* chest xray bilat infiltrates
* non-cardiogenic pulmonary edema
**Oxygenation: PF ratio **
* mild: 201-300 mmHg
* moderate: 101-200
* severe: less than 100
How do you treat / manage ARDS?
Treat the hypoxemia
Protect the lung - limit plateau pressure
Explain Permissive (hypoventilation) hypernapnia
Lowers tidal volume requiring less pressure to rise CO2 and drop pH
What ventilator settings can be adjusted to treat low pCO2?
Increase resp. rate to blow off more CO2
What is a pleural effusion?
Collection of serous fluid in pleural cavity
* result of underlying cause
* an imbalance of production & fluid removal
Lots of fluid compresses lung; non-compliant
What are the types of pleural effusion?
Exudative
* increase in capillary wall permeability
* both fluid and proteins move into pleural space, pulling water with it (oncotic pull)
Transudative
* just fluid moves due to hydrostatic pressure
* decrease in oncotic pressure & no protein
What are the assessment findings for pleural effusion?
Inspection
* increase RR, SOB, accessory muscle use
Palpation
* chest expansion
* tracheal shift possible
Auscultation
* pleural friction rub
* decreased breath sounds
Pain
* pleuritic, worse with inspiration
ABG
* respiratory alkalosis / acidosis
* metabolic acidosis
What would be the treatment for pleural effusion?
Thoracentesis
