Respiratory Pathophys Flashcards
What is a pulmonary embolus
Occlusion of a portion of pulmonary artery circulation by an embolus, disrupting blood flow to lungs and decreasing gas exchange
What are the two types of pulmonary embolus?
1) Thrombotic embolus (blood clot)
2) Non-thrombotic embolus (fat, amniotic fluid, air)
Where do the majority of PE’s come from?
DVT from legs (thrombotic)
Where does a thrombotic PE occlude blood flow?
From the pulmonary artery to the pulmonary vein (preventing blood from getting to lungs for gas exchange)
What are the 3 classifications of PE?
1) Massive PE
2) Submassive PE
3) Low risk PE
What is a massive PE?
Acute PE with sustained hypotension (<90mmHg or 40mmHg drop from baseline), tissue hypoperfusion, hypoxemia.
Must rule out MI before starting inotropes
How do pts die from massive PE? Heart issues or lung issues
Pts die from RV failure.
Dual blood circulation in lungs from the bronchiole + pulmonary arteries make lung infarct unlikely
What is a submassive PE?
Acute PE with stable hemodynamic status but evidence of RV dysfunction or myocardial necrosis
What is a low risk PE?
Normal BP, no RV dysfunction or signs of MI
What are the risk factors for PE?
VIRCHOW’S TRIAD
1) Venous stasis
2) Hypercoagulability
3) Vessel damage
What can cause venous stasis?
Immobility, NMBAs, illness, pregnancy, AFIB, increased estrogen, obesity
What can cause hypercoagulability?
Oral contraceptives, estrogens, coag disorders
What can cause vessel damage that increases risk of PE?
Trauma, surgery, atherosclerosis, inflammation
What are the 4 things that happen (pathophys) during massive PE?
1) Increased deadspace in the affected lung (alveolar deadspace)
2) Bronchoconstriction in the affected lung (compensatory mechanism)
3) Compensatory shunting to the unaffected lung (V/Q mismatch)
4) Hemodynamic changes (pulmonary hypertension due to flow obstruction)
- -> Mediators released at site of clot causes pulmonary vasoconstriction
Why do the lungs bronchoconstrict during massive PE?
Low perfusion to the lung means low CO2 is carried up to alveoli. Compensatory bronchoconstriction kicks in to help pt retain CO2 as body thinks serum CO2 is low
What are the causes of RV failure as a result of massive PE?
1) Flow obstruction in pulmonary artery causes pulmonary hypertension
2) Increased workload for RV due to increased afterload
3) Decreased preload at the L ventricle decreases CO and BP
4) Too much blood backs up into RV, not enough O2, RV dilates, cells die
What is the effect of the mediators released from the PE clot?
Pulmonary vasoconstriction from the clot mediators on top of compensatory pulmonary vasoconstriction in hypoxemia makes hypoxia and pulmonary hypertension worse
How is PE diagnosed?
Spiral CT with contrast
Required for definitive diagnosis: Pulmonary angiography, V/Q scan (cannot do if vented)
CXR, echocardiogram (assess RV)
Doppler (Assess DVT)
ABGs
What are ABG changes associated with massive PE/
Initially resp alkalosis then combined acidosis from anaerobic metabolism and resp failure
What are assessment findings related with massive PE?
Resp distress, pleuritic chest pain, cough, signs of DVT, distended neck veins, ventricular arrythmias, tachycardia, crackles, decreased breath sounds
What is medical management for PE?
Ventilation, hemodynamic management, anticoags, thrombolytic agents (only for massive PE, best given within 48hrs)
Catheter directed treatment, surgical embolectomy, IVC filter
What is a pneumothorax?
Accumulation of BLOOD or AIR in the pleural space
What are the 3 types of pneumothorax?
1) Open pneumo
2) Closed pneumo
3) Tension pneumo
What is an open pneumo and what can cause it?
Opening in the pleural cavity by laceration to chest wall or parietal pleura. Air enters the space.
Can be caused by trauma, central line insertion, rib fractures
What is a closed pneumo and what can cause it?
No disruption to parietal pleura but visceral pleura is torn
Can be caused by alveolar rupture, blunt chest wall trauma, pneumonia, emphysema “blebs”
What is a tension pneumothorax and what can cause it?
Air enters pleural space on inspiration but cannot exit on expiration. More air builds up and causes lung collapse and mediastinal shift.
Can be caused by both open and closed pneumo
Why is mediastinal shift bad?
Compresses the heart and other lung will also collapse
What is pathophys for open or closed pneumo?
1) Air enters pleural space
2) Affected lung compressed, collapses
3) Alveoli underventilation
What is pathophys for tension pneumo?
1) Pressure in pleural space increases
2) Affected lung collapses, causing mediastinal shift
3) Decreased preload, CO from pressure on major vessels
4) Unaffected lung also collapses
What are key assessments for pneumo?
Decreased chest expansion on affected side, resp distress, subcutaneous emphysema, tracheal deviation, hyper-resonance and decreased breath sounds on affected side
What is diagnosis for pneumo?
CXR
What is medical intervention for pneumo?
Treatment usually required if pneumo > 15% of lungs
Needle thoracentesis for tension pneumo
Chest tube
Ventilation
Where is the needle inserted for needle thoracentesis?
Affected side at 2nd ICS, midclavicular line
What is pulmonary edema?
Abnormal accumulation of fluid in alveoli and interstitial spaces of lungs
What are the 2 types of pulmonary edema?
1) Cardiogenic pulmonary edema
2) Non-cardiogenic pulmonary edema
What causes cardiogenic pulmonary edema?
Increased hydrostatic pressure
Dysfunction of LV or LV failure causes blood to back up into the LA and pulmonary veins, then eventually pulmonary carpillaries and into the alveoli
Hydrostatic pressure causes fluid to be pushed out of pulmonary capillaries
Can also be caused by cardiomyopathies, valvular stenosis (mitral, aortic), MI
What causes non-cardiogenic pulmonary edema
Cardiac function is normal but there is increased capillary permeability in the lungs causing fluid and proteins to shift into interstitium
Caused by:
Infection, inflammation, sepsis, aspiration, multiple blood transfusions, LYMPH INSUFFICIENCY (inadequate drainage), LOW SERUM ALBUMIN (decreased colloidal oncotic pressure)
What are the stages of pulmonary edema and what happens?
Stage 1 –> Fluid moves into interstitium, lymphatic vessels still able to remove excess fluids. Alveoli remain dry
Stage 2 –> Interstitial pulmonary edema. Lymphatic system is overworked, fluid accumulates in interstitium impairing gas exchange
Stage 3 –> Alveolar pulmonary edema. Alveoli are filled and will collapse creating shunt like units. Crackles heard
What are key assessments for pulmonary edema?
Onset may be gradual or sudden. Early signs are cough.
Resp distress, anxiety, distended neck veins, blood tinged sputum, tachycardia. Cool extremities, weak pulses, edema. Lung crackles, decreased air entry, S3, S4
What are ABG changes in pulmonary edema?
Initially increased RR leads to resp alkalosis then fatigue causes CO2 retention and resp acidosis.
Anaerobic metabolism leads to metabolic then combined acidosis
How is pulmonary edema diagnosed?
CXR (identify cardiogenic, view cardiac silhouette)
Echocardiogram (Assess LV, valvular function)
What is ventilation treatment for pulmonary edema?
BIPAP, EPAP, CPAP
Ventilation / PEEP to prevent fatigue, alveolar collapse, decrease fluid shifts into the lungs
Why does PEEP help pulmonary edema?
Decreases preload, decreases hydrostatic pressure and fluid shifts into the lungs
What are medications for cardiogenic pulmonary edema?
Vasodilators (nitroglycerin) decreases hydrostatic pressure
Diuretics (shift blood out of lungs)
Inotrops (if decreased FOC), benzos, morphine given cautiously
What is treatment for non-cardiogenic PE?
Infection control, diuretics, treat underlying cause
What is pleural effusion?
Collection of serious fluid in the pleural cavity, results from another disease process
Normal amount of fluid in pleural cavity is 30-50cc
What are the 2 types of pleural effusion?
1) Transudate effusion
2) Exudate effusion
What is transudate effusion and what causes it?
Fluid leaks through capillary membrane into pleural space due to:
1) Increased hydrostatic pressure (HF, fluid overload)
2) Decreased colloid oncotic pressure (liver failure)
What is exudate effusion and what causes it?
Fluid, albumin, plasma proteins leak through capillary membranes that have increased permeability. (Pneumonia, pancreatitis)
This causes an oncotic pull which worsens the effusion.
What happens if pleural effusion is prolonged or infected?
Becomes gel like and difficult to aspirate, becomes “empyema”
What is pathophys of pleural effusion?
1) Fluid passes into pleural cavity
2) Decreased lung expansion, decreased compliance
3) Compression atelectasis
4) Empyema, fluid gels up
5) Fibrosis
What are key assessments for pleural effusion?
If effusion < 300cc, pts can be asymptomatic
Resp distress, decreased chest expansion on affected side, mediastinal shift, dull/flat over affected side, pleural friction rub, decreased breath sounds, pleuritic chest pain worse on inspiration
How is pleural effusion diagnosed?
CXR (best in upright position)
How is pleural effusion treated?
Treatment usually required if effusion > 500cc
Monitor resp distress, infection control (infections make vessels more permeable), vent mode depends on amount of fluid (PSV –> ACPC), thoracentesis (send cultures), chest tube insertion for large effusions
What is ventilator associated pneumonia?
Subgroup of nosocomial acquired pneumonia, develops 48-72 hrs post intubation. Commonly caused by staph A, pseudomonas, ecoli
What are predisposing risk factors to VAP?
Mechanical ventilation, reintubation, decreased LOC, immobility, decreased gag/cough, supine positioning, NGT, aspiration, immunosuppression, histamine blockers, smoker, pre-existing lung disease, sepsis
What is the pathophys for VAP?
1) Type III alveolar cells attack pathogens that make their way into lungs
2) Damaged cells secrete cytokines causing capillary vasodilation and increased permeability
3) WBCs and fluids leak out of capillary into alveoli
5) Alveoli become filled with pus (CAPILLARY SHUNT)
What are key assessments for VAP?
Timing, CXR showing new consolidations in lungs, increased WBCs, worsening ABGs, productive cough, thick purulent sputum, increased temp, dullness over consolidation, crackles, bronchial breath sounds, decreased air entry
How is VAP diagnosed?
CXR (consolidation, infiltrates, new opacities)
WBCs elevated > 12000 or < 4000 OR T > 38 with no cause
Secretions, suctioning needs, breath sounds, worsening P/F ratio, sputum cultures postiive
What are some things in the VAP prevention bundle and nursing management?
1) Prevent aspiration –> HOB 30-45 degrees, oral care, clear secretions, cuff pressure, subglottic ETT, assess extubation, mobility
2) Prevent colonization –> Oral decontam, asceptic closed suctioning, HME, vent circuit change when needed
3) Other –> Hand washing, DVT prophylaxis, enteral feeding within 24-48 hrs of admission
How is VAP treated?
Antibiotics, AC/PC, mobilization, nutrition
