Vascular Lung Disorders
Pulmonary edema- accumulation of fluid in alveoli and interstitial lung spaces; interferes with
gas exchange; and is considered a Medical Emergency.
oComplication s many diseases of the heart, lungs and liver or malignancies
oMost common is left sided Heart Failure
oPg. 577 table 28-28
Pulmonary embolism-
oEtiology & patho- blockage of the pulmonary arteries that blocks perfusion of the alveoli
(thrombus, fat, air, or tissue becomes dislodged and travels to the lungs where it lodges
in a vessel and obstructs blood flow to the lungs) massive PE can be fatal.
DVT is most common
VTE
Thrombus: r side of heart, atrial fibrillation
Fat emboli: fractured long bones
Air emboli: improper IV admin.
Bacterial vegetation
Amniotic fluid
Tumors
oS&S- easily misdiagnosed, undetected and untreated
Risk factors: immobilization, increased age, surgery in last 3 months, HTN,
Stroke, CVD, family history of DVT, malignancy, Women: obese, smokers, HTN,
oral contraceptives, pregnancy, and HRT. ! in 5 patients admitted with COPD
exacerbation may also have PE
Symptoms: anxiety, dyspnea, tachypnea, tachycardia, pleuric chest pain, cough,
hemoptysis, hypoxemia;
oComplications
Massive blockage = shock, pulmonary infarction: tissue death
Small/multi emboli: pulmonary hypertension, cor pulmonale
Recurrent emboli result in chronic pulmonary hypertension which results in
dilation & hypertrophy of the Right ventricle
oDiagnostic- Spiral (helical) CT scan most frequently used test to diagnose PE. Involves
injecting contrast media in order to visualize blood vessels.
If a patient cannot have contrast a V/Q scan is done (inholes radioscopy and
inhalation of xenon)
D-dimers – to measure amount of cross linked fibrin fragments.
Venous ultrasound
Pulmonary angiogram- Invasive procedure involving a insertion of a catheter into
the femoral or antecubital vein & injection of contrast medium to allow
visualization of the pulmonary vascular system and location of the embolus.
ABG analysis is important but not diagnostic. The PaO2 is low b/c of inadequate
oxygenation 2ndary to an occluded pulmonary vasculature preventing matching
of perfusion to ventilation.
Chest x-rays and EKG also important data collection pieces but not diagnostic.
oCollaborative care- prevention of PE starts w/ prevention of DVT: prophylactic use of
anticoagulant meds, uses of SCDs, and early ambulation.
Drug therapy-
heparin ( lovenox) warfarin (Coumadin): used in prevention,
tPA or alteplase (activase) used to dissolve
Surgical therapy- interior vena cava (IVC) filter- filtration of clots without
interruption of blood flow. Used for patients who are high risk and have
contraindications for anticoagulant therapy.
Embolectomy is rare, 50% mortality rate.
Nursing diagnoses: impaired gas exchange, ineffective tissue perfusion,
decreased cardiac output, pain & anxiety, therapeutic regimen management,
risk for injury
Nursing interventions- minimal sedation, DVT prophylaxis early removal of
central venous lines, assessment and auscultation, monitor vitals w/ O2
saturations, monitor ABGs, supplemental O2, bedrest in semi fowlers,
Encourage turn cough, and deep breathing, incentive spirometry, use SCDs,
manage pain levels, educate for discharge about prevention and follow up care
Pulmonary hypertension- related to pulmonary vascular resistance to blood flow
oPPH- Primary
oSPH- seconday
oCauses= (PPH possibly) genetic= lung disease (alveolar hypoxia, fibrosis) LV dysfunction,
PE, and systemic connective tissue disease. (SPH)
oSymptoms= progressive dyspnea on exertion; fatigue and legargy, exacerbation with
exercise, exertional chest pain, dizziness, syncope.
Symptoms related to the inability of cardiac output to increase in response to
oxygenation demands.
Eventually as disease progresses will have dyspnea at rest.
A remodeling (thickening of the walls) of the vessels occurs, which increases
vascular resistance and pulmonary pressure.
oTreatments- no cure for PPH but treatment can relieve symptoms, increase quality of life
and prolong life.
Diuretics to relive dyspnea, peripheral edema, and right ventricle overload
Anticoagulants to prevent thrombus
Low flow O2 to relieve hypoxia
Vasodilator therapy: Ca channel blockers
Newer meds: Prostacyclins (pulmonary vasodilation and reduce vasculature
resistance.
COR PULMONALE- enlargement of the right ventricle secondary to diseases of the lung, thorax,
or pulmonary circulation.
oPPH is usually a preexisting condition in the individual with cor pulmonale.
May be present with or without overt cardiac failure.
Most common cause is COPD
oS&S: dyspnea and fatigue, chronic productive cough, wheezing, substernal pain.
Chronic hypoxemia may lead to polycythemia
If heart failure accompanies cor pulmonale additional S&S: peripheral edema,
weight gain distended neck veins, full bounding pulse, and enlarged liver will
also be found. A chest X-ray will show an enlarged right ventricle and pulmonary
artery.
oTreatment- primary management is treatment of the underlying pulmonary disease.
Long term low flow O2 therapy
Correction of F&E imbalances
Similar treatments as PPH
Phlebotomy is indicated in patients w/ chronic cor pulmonale& chronic
hypoxemia causing severe polycythemia. (Hct >65%)
Lung transplantation- end stage Lung disease, prolong survival and quality of life.
oLimiting factor is # of donors.
oExtensive evaluations
oHigh risk for infection (leading cause of death)
oHigher levels of immunosuppressant compared to other organ transplants (strict
combination therapy)
oRehab to increase endurance
oTeaching – focused on family, role changes
oAcute rejection is common
EBP: the earlier the onset of chronic rejection or the need for O2 at home, the
shorter the period of survival.
Risk for death increased 37% in patient over 60
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