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CCN > Respiratory Pathophys > Flashcards

Respiratory Pathophys Flashcards

1
Q

What is a pulmonary embolus

A

Occlusion of a portion of pulmonary artery circulation by an embolus, disrupting blood flow to lungs and decreasing gas exchange

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2
Q

What are the two types of pulmonary embolus?

A

1) Thrombotic embolus (blood clot)

2) Non-thrombotic embolus (fat, amniotic fluid, air)

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3
Q

Where do the majority of PE’s come from?

A

DVT from legs (thrombotic)

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4
Q

Where does a thrombotic PE occlude blood flow?

A

From the pulmonary artery to the pulmonary vein (preventing blood from getting to lungs for gas exchange)

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5
Q

What are the 3 classifications of PE?

A

1) Massive PE
2) Submassive PE
3) Low risk PE

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6
Q

What is a massive PE?

A

Acute PE with sustained hypotension (<90mmHg or 40mmHg drop from baseline), tissue hypoperfusion, hypoxemia.

Must rule out MI before starting inotropes

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7
Q

How do pts die from massive PE? Heart issues or lung issues

A

Pts die from RV failure.

Dual blood circulation in lungs from the bronchiole + pulmonary arteries make lung infarct unlikely

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8
Q

What is a submassive PE?

A

Acute PE with stable hemodynamic status but evidence of RV dysfunction or myocardial necrosis

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9
Q

What is a low risk PE?

A

Normal BP, no RV dysfunction or signs of MI

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10
Q

What are the risk factors for PE?

A

VIRCHOW’S TRIAD

1) Venous stasis
2) Hypercoagulability
3) Vessel damage

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11
Q

What can cause venous stasis?

A

Immobility, NMBAs, illness, pregnancy, AFIB, increased estrogen, obesity

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12
Q

What can cause hypercoagulability?

A

Oral contraceptives, estrogens, coag disorders

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13
Q

What can cause vessel damage that increases risk of PE?

A

Trauma, surgery, atherosclerosis, inflammation

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14
Q

What are the 4 things that happen (pathophys) during massive PE?

A

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

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15
Q

Why do the lungs bronchoconstrict during massive PE?

A

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

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16
Q

What are the causes of RV failure as a result of massive PE?

A

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

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17
Q

What is the effect of the mediators released from the PE clot?

A

Pulmonary vasoconstriction from the clot mediators on top of compensatory pulmonary vasoconstriction in hypoxemia makes hypoxia and pulmonary hypertension worse

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18
Q

How is PE diagnosed?

A

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

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19
Q

What are ABG changes associated with massive PE/

A

Initially resp alkalosis then combined acidosis from anaerobic metabolism and resp failure

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20
Q

What are assessment findings related with massive PE?

A

Resp distress, pleuritic chest pain, cough, signs of DVT, distended neck veins, ventricular arrythmias, tachycardia, crackles, decreased breath sounds

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21
Q

What is medical management for PE?

A

Ventilation, hemodynamic management, anticoags, thrombolytic agents (only for massive PE, best given within 48hrs)

Catheter directed treatment, surgical embolectomy, IVC filter

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22
Q

What is a pneumothorax?

A

Accumulation of BLOOD or AIR in the pleural space

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23
Q

What are the 3 types of pneumothorax?

A

1) Open pneumo
2) Closed pneumo
3) Tension pneumo

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24
Q

What is an open pneumo and what can cause it?

A

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

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25
Q

What is a closed pneumo and what can cause it?

A

No disruption to parietal pleura but visceral pleura is torn

Can be caused by alveolar rupture, blunt chest wall trauma, pneumonia, emphysema “blebs”

26
Q

What is a tension pneumothorax and what can cause it?

A

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

27
Q

Why is mediastinal shift bad?

A

Compresses the heart and other lung will also collapse

28
Q

What is pathophys for open or closed pneumo?

A

1) Air enters pleural space
2) Affected lung compressed, collapses
3) Alveoli underventilation

29
Q

What is pathophys for tension pneumo?

A

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

30
Q

What are key assessments for pneumo?

A

Decreased chest expansion on affected side, resp distress, subcutaneous emphysema, tracheal deviation, hyper-resonance and decreased breath sounds on affected side

31
Q

What is diagnosis for pneumo?

A

CXR

32
Q

What is medical intervention for pneumo?

A

Treatment usually required if pneumo > 15% of lungs

Needle thoracentesis for tension pneumo

Chest tube
Ventilation

33
Q

Where is the needle inserted for needle thoracentesis?

A

Affected side at 2nd ICS, midclavicular line

34
Q

What is pulmonary edema?

A

Abnormal accumulation of fluid in alveoli and interstitial spaces of lungs

35
Q

What are the 2 types of pulmonary edema?

A

1) Cardiogenic pulmonary edema

2) Non-cardiogenic pulmonary edema

36
Q

What causes cardiogenic pulmonary edema?

A

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

37
Q

What causes non-cardiogenic pulmonary edema

A

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)

38
Q

What are the stages of pulmonary edema and what happens?

A

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

39
Q

What are key assessments for pulmonary edema?

A

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

40
Q

What are ABG changes in pulmonary edema?

A

Initially increased RR leads to resp alkalosis then fatigue causes CO2 retention and resp acidosis.

Anaerobic metabolism leads to metabolic then combined acidosis

41
Q

How is pulmonary edema diagnosed?

A

CXR (identify cardiogenic, view cardiac silhouette)

Echocardiogram (Assess LV, valvular function)

42
Q

What is ventilation treatment for pulmonary edema?

A

BIPAP, EPAP, CPAP

Ventilation / PEEP to prevent fatigue, alveolar collapse, decrease fluid shifts into the lungs

43
Q

Why does PEEP help pulmonary edema?

A

Decreases preload, decreases hydrostatic pressure and fluid shifts into the lungs

44
Q

What are medications for cardiogenic pulmonary edema?

A

Vasodilators (nitroglycerin) decreases hydrostatic pressure

Diuretics (shift blood out of lungs)

Inotrops (if decreased FOC), benzos, morphine given cautiously

45
Q

What is treatment for non-cardiogenic PE?

A

Infection control, diuretics, treat underlying cause

46
Q

What is pleural effusion?

A

Collection of serious fluid in the pleural cavity, results from another disease process

Normal amount of fluid in pleural cavity is 30-50cc

47
Q

What are the 2 types of pleural effusion?

A

1) Transudate effusion

2) Exudate effusion

48
Q

What is transudate effusion and what causes it?

A

Fluid leaks through capillary membrane into pleural space due to:

1) Increased hydrostatic pressure (HF, fluid overload)
2) Decreased colloid oncotic pressure (liver failure)

49
Q

What is exudate effusion and what causes it?

A

Fluid, albumin, plasma proteins leak through capillary membranes that have increased permeability. (Pneumonia, pancreatitis)

This causes an oncotic pull which worsens the effusion.

50
Q

What happens if pleural effusion is prolonged or infected?

A

Becomes gel like and difficult to aspirate, becomes “empyema”

51
Q

What is pathophys of pleural effusion?

A

1) Fluid passes into pleural cavity
2) Decreased lung expansion, decreased compliance
3) Compression atelectasis
4) Empyema, fluid gels up
5) Fibrosis

52
Q

What are key assessments for pleural effusion?

A

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

53
Q

How is pleural effusion diagnosed?

A

CXR (best in upright position)

54
Q

How is pleural effusion treated?

A

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

55
Q

What is ventilator associated pneumonia?

A

Subgroup of nosocomial acquired pneumonia, develops 48-72 hrs post intubation. Commonly caused by staph A, pseudomonas, ecoli

56
Q

What are predisposing risk factors to VAP?

A

Mechanical ventilation, reintubation, decreased LOC, immobility, decreased gag/cough, supine positioning, NGT, aspiration, immunosuppression, histamine blockers, smoker, pre-existing lung disease, sepsis

57
Q

What is the pathophys for VAP?

A

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)

58
Q

What are key assessments for VAP?

A

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

59
Q

How is VAP diagnosed?

A

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

60
Q

What are some things in the VAP prevention bundle and nursing management?

A

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

61
Q

How is VAP treated?

A

Antibiotics, AC/PC, mobilization, nutrition

CCN (27 decks)

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