Pulmonary Edema: Common Causes
2.Overhydratiion with IV (too much especially with HF. Be conscientious when you’re giving pt with hx of hf or current hf IV flluids)
3.Hypoalbuminemia: (Nephrotic syndrome, Hepatic disease, nutritional disorders). Dealing with albumin levels of the pt
4.Altered capillary permeability of lungs: inhaled toxins, inflammations (ex pneumonia), severe hypoxia, near-drowing. (maybe they’ve inhaled a substance that causes inflammatory process to occur—fluid build up in lung)
5.Malignancies of the lymph system in the lungs
6.Respiratory distress syndrome (oxygen toxicity): over oxygenation. ICU, the first time they’re very hypoxic but then the next ABG’s; 110-130%, so they need to back down on oxygenation
7.Unknown causes: neurogenic condtion, opioid overdose, reexpansion pulmonary edema, and high altitudes
8.-Neuro: Inability to breathe due to neurological changes.
9.-High altitude: lung problems and heart problems. Higher elevations have less oxygen supply, so more RBC and H&H are much higher because there is less oxygen (a protection mechanism). So it spreads the oxygen around. When altitude changes, the rush of fluid goes into lungs. If you’re overly hydrated, then you will decrease your RBC and H/H levels which is BAD because this makes oxygenation difficult. Dehydrations allows you to better accommodate. Diamox diuretic helps with that RBC shift before.
- Pulmonary edema is a life-threatening event that canresult from severe heart failure. In pulmonary edema, theleft ventricle fails to eject sufficient blood, and pressureincreases in the lungs because of the accumulated blood.The client is immediately placed in a high Fowler’s position,with the legs in a dependent position, to reduce pulmonarycongestion and relieve edema. Oxygen is alwaysprescribed, usually in high concentrations by mask or cannulato improve gas exchange and pulmonary function; thegoal is to keep the oxygen saturation above 90%. The clientis then assessed quickly, including checking the lungsounds.
- Next it is important to ensure that an IV access device is in place for the administration of a diuretic andmorphine sulfate.
- Furosemide, a rapid-acting diuretic, willeliminate accumulated fluid.
- Morphine sulfate reducesvenous return (preload), decreases anxiety, and also reduces the work of breathing.
A Foley catheter is insertedto measure output accurately. The nurse then prepares forintubation and ventilator support, if required. The nurse stays with the client and provides reassurance.
Vital sign sare monitored and a cardiac monitor is used to monitor theheart rate and for dysrhythmias.
The lung sounds are monitoredfor crackles, decreased breath sounds, and for aresponse to treatment.
A weight measurement will also determine a response to treatment.
Other interventions may include the administration of digoxin to increase ventricular contractility and improve cardiac output, bronchodilators for severe bronchospasm or bronchoconstriction,medications to facilitate myocardial contractility and enhance stroke volume, and vasodilators to reduce afterload,increase the capacity of the systemic venous bed,and decrease venous return to the heart. The nurse finallydocuments the event, actions taken, and the client’sresponse.
Pulmonary Embolism: Etiology
Mortality rate of 30% when not treated (down to <8% with therapy)
Majority of PE’s are from DVT with most lethal originating in the femoral or iliac veins
Spinal cord injuries are at highest risk for developing DVT
Fat emboli common with long bone surgeries
Thrombi from A-fib may also lead to PE
Air emboli occur from non-primed IV tubing
- Other Notes:
- With treatment, still a high mortality rate
Most common cause: from a DVT secondary to Post sx complications
Truck drivers: long drives, get up and they have chest pain. They should be walking around But they have poor diet and health factors
Spinal cord injuries:
highest risk for developing DVTs. Ask when they had that last sx: that window time that increases incidence of DVT that becomes PE
Especially long bones: hips, femurs, arm sx
A fib thrombi:
blood starts turning around in that atrium, clots form and become big enough they go right into coronary system or even a CVA
- Air emboli: non primed IV tubing. About 20 ml. That whole 20 mL air must get into pt to cause an emboli. Glamorized on TV that one little bubble will result in emboli.
- -10 mL can cause air emboli
Pulm Embolism Patho & Risk Factors
Spontaneous dislodgement of thrombi in deep veins or from mechanical forces such as BP changes (High change in BP or a low change to high.. It can dislodge those clots very easily)
Majority pt’s with PE have no leg (DVT) symptoms (usually they don’t have that Homan’s sign.. Occassionallly they can check that Homans. Positive = great save.)
Spinal cord injuries are at highest risk for developing DVT
- Risk factors
- Surgery in last 3 mo. (especially pelvic/lower extremity): spinal cords injuries
- Spinal injury
Hx of DVT: even if pregnant women, increase in blood volume, change in vasc oncotic pressure increases their risk of DVT. If they actually do have a DVT, that puts them at risk for MORE DVTs in the future.
Clinical Manifestations of PE:
- Triad (occur in 20% of pts.): comes on RAPID!
- Dysnpea (difficulty breathing)
- Chest pain (crushing)
- Hemoptysis (last to be seen: coughing up sputum)
- Pleuritic chest pain
- Pulmonic heart sounds: sounds like air sounds going through. Air exchange sound.
Sudden change in mentation (LOC changes sudden)
- Massive (33% mortality) High mortality rates
- Severe dyspnea
Diagnostics & Complications of PE
- 1. Pulmonary infarction: No oxygen exchange at ALL.
2. Pulm HTN:
- Pulm Embolism Diagnostics
- X-ray at bedside immediately
- ABG’s Do these first
- Spiral CT scan
- V/Q scan
- D-dimer Positive when pt. has a DVT, MI, unstable angina or stroke-Can be positive with other things, so it’s not specific. They’re complaining of chest pain anyways.
PE Collaborative Care & Surgical Therapy
- Drug Therapy
- Fibrinolytic agents
- Anticoagulant therapy
Oxygen: If dyspnea
IV fluid therapy replacement and/or vasopressors for s/s shock
Diuretics for HF
Narcotics for pain control
put on antithrombotic agent. Maybe Fibrinolytic agent: clot buster!
Antiocagulagnts based on symptomology (depends on size, location and symptoms)-
: PTT. Antidote: Protamin Sulfate. Watch platelets because of HIT.
: platelets (look for lowering plts to see if it’s working). H&H (not changing anything based on this), also can look at Cr.Cl.
when transitioning from IV to oral. Look for PT and INR. Antidote: Vit K.
Other drugs: Plavix. Xarelto (no lab values. Nice thing.)
- For a procedure:
- On Coumadin: stop 2-3 days before
- Lovenox: 12-24 hours stop (good thing)
- Xarelto: stop before 3 days.
If It’s so bad that they need to do embolectomy: surgical approach.
Inferior Vena Cava (IVC):
small clots that are scattered throughout lower extremeites; helps collect. Doesn’t stay in forever. They will schedule a removal eventually.
Pulmonary Embolism: Nursing Managment
- Post op day 1 and chest pain!
- Sit the pt down.
- Oxygenate And Bring Cashcart and hook up to the monitor.
- Elevate HOB.
- Call Rapid Response right away. We need immediate intervention. Assume it’s a PE!
- Health promotion: Decreasing risk factors, Prophylaxis with high risk categories
- -age, weight, comorbidities, vascular problems, diet, BP control, Past hx of sx interventions. Trauma.
-Prophylaxis: baby aspirin or regular 325. Life long Coumadin/Plavix/xarelto. Or if they’ve had hx of DVT, they’ll prophylactically make the pt take Lovenox A WEEK before the sx and a week after. So it depends on the situation.
- Acute intervention: Immediately post op Days 1-3
- HOB high fowlers: Sit your patients down if they’re walking. HOB all the way up.
- IV access
- O2 therapy: If dyspnic. Difficulty breathing
- Monitoring of: EKG, Lung sounds, ABG’s, VS, Labs, Medication effects. Call for cxr and labs
- Anxiety control: Feel like pressure they can’t breathe, grasping for air. Narcotic or antianxiety agent.
- Bed rest: once we get a dx, these individuals will be in bed rest. Identify what kind? Bed rest bathroom privileges? Or bed rest with commode ? Or just strict BedRest depending on PE, where it’s located and the susceptibility of it dislodging.
No VTE prophylaxis on affected limb
If a DVT is already indentified on a lower ext, make sure SCD and Ted is not on that AFFECTED extremity, but is on the UNAFFECTED SIDE.
- Ambulatory and home care : Anticoagulation management and precautions
- -Education of mamangament and symptomology recognition
- -Their knowledge of anticoagulation and precautions when they go home.
- Teaching about med side effects but also drug-drug and drug-food interactions.
- Most facilities have thise list with anticoagulant interactions to give the pt.
PULMONARY HYPERTENSION: Etiology
-Anticoagulants prevent clots from growing. Doesn’t make it grow smaller (that’s the body’s action)
-Meds to make clot smaller: fibrolytic therapy. The Clot buster.
-TPA: No time window (this is more for CVA.) When you recognize PE, it should be given immediately. Based on clot size, location and doctor’s judgement
THIS PE inside lungs is blocking blood flow, increasing the blood pressure within our lungs, Causing pulmonary htn --> R Vent Hypertrophy -->Cor Pulmonale (R Sided HF)
Elevated pulmonary pressures due to an increase in pulmonary vascular resistance (such as a P.E.) , classified as primary or secondary (complication from a co-morbidity)
- Primary: when we have pulm artery pressure (normally at rest is 14) but higher at rest indicates Pulm htn (PAP: Pulmonary Artery Pressure)
- PAP >25 mm Hg at rest
- PAP >30 mm Hg with exercise and no underlying cause
- Increased Vascular resistance caused by
- Pulmonary vessel remodeling/thickening: LIKE IN COPD. ARDS --> Vessel thickening.
- Thrombosis in situ (just sitting there)
Pulm HTN Clinical Manifestations & Diagnostic Studies
- Dyspnea on exertion: when they’re exercising
- Exertional chest pain: exercising
- Right ventricle hypertrophy (cor pulmonale)
- Diagnostic Studies
- Rule of exclusions since this would look like a lot of other things
- Positive for
- Enlarged central pulmonary arteries
- Clear lung fields
- Right ventricular hypertrophy (cxr for size of heart, and silhouette for enlargement)
- Increased pulmonary artery pressures
Pulm HTN Treatment
Prevent progression to HF
- -Focused on symptomology
- -Poor oxygenation: give O2
- -Too much Fluids: give diuretics-Decrease the vascular resistance
- Drug therapy to
- Produce vasodilation of pulmonary vessels
- Reduce right ventricular overload
- Reverse remodeling
- Surgical relief If drug therapy doesn’t work.
- Atrial septostomy
- Pulmonary thromboendarterectomy: take out thrombous
- Lung transplantation: If it’s soooo bad, to the point that we can’t control what’s going on. Take out either portion, a size or just a lobe itself.
Secondary Pulm htn:
-Relative to other factors that a patient has control over.
-Diagnosed the same, but looking at symptomology and causes and reversing these causes.
-Treatment is pretty much the same: manange the underlying disease process that’s causing it
-We want too minimize the chance of it going into Cor Pulmonale.
Increase in PAP due to a primary/chronic disease: Symptoms mimic the primary/chronic disease
: Same as Primary Pulmonary Hypertension
- Management of underlying disease, If irreversible damage occurs, institute Primary Pulmonary Hypertension treatment modalities
Cor Pulmonale S/S
Lung disorders cause pulmonary hypertension by several mechanisms:
Loss of capillary beds (eg, due to bullous changes in COPD or thrombosis in pulmonary embolism)
Vasoconstriction caused by hypoxia, hypercapnia, or both
Increased alveolar pressure (eg, in COPD, during mechanical ventilation)
Medial hypertrophy in arterioles (often a response to pulmonary hypertension due to other mechanisms)
Pulmonary hypertension increases afterload on the RV, resulting in a cascade of events that is similar to what occurs in LV failure, including elevated end-diastolic and central venous pressure and ventricular hypertrophy and dilation. Demands on the RV may be intensified by increased blood viscosity due to hypoxia-induced polycythemia.
- Symptoms and Signs
- Initially, cor pulmonale is asymptomatic, although patients usually have significant symptoms (eg, dyspnea, exertional fatigue) due to the underlying lung disorder. Later, as RV pressures increase, physical signs commonly include a left parasternal systolic lift, a loud pulmonic component of the 2nd heart sound (S 2 ), and murmurs of functional tricuspid and pulmonic insufficiency. Later, an RV gallop rhythm (3rd [S 3 ] and 4th [S 4 ] heart sounds) augmented during inspiration, distended jugular veins (with a dominant a wave unless tricuspid regurgitation is present), hepatomegaly, and lower-extremity edema may occur.
Cor Pulmonale Diagnostics & Collaborative Care
H/P, through ABGs, serum electrolyes, EKG, Chest Xray.
- Collaborative Care: Give oxygen, Bronchodilators, Diuretics , Low Sodium Diet to decrease BP.
- Vasodilators if indicated can help with general blockage.
- (same therapy as pulm htn, but continue this therapy.)
- Cor Pulm Interventions:
- Listen to the patient’s fears and concerns about his illness.
- Plan a nutritious diet carefully with the patient and the staff dietitian.
- Prevent fluid retention by limiting the patient’s fluid intake to 1,000 to 2,000 ml daily and providing a low sodium diet.
- Reposition the bed ridden patient often to prevent atelectasis.
- Provide meticulous respiratory care, including oxygen therapy and for COPD patients.
- Pace patient care activities to avoid patient fatigue.
- Monitor serum potassium levels closely if the patient takes a diuretic.
- Be alert for complaints that signal digoxin toxicity, such as anorexia, nausea, vomiting, and seeing a yellow halo around an object.
- Measure ABG levels and watch for signs of respiratory failure as change in pulse rate, deep labored respirations; and increased fatigue produced by exertion.
- Instruct the patient to schedule frequent rest periods and to perform his breathing exercises regularly.
Common indications for Lung Transplation
Idiopathic Pulmonary Fibrosis
Cystic Fibrosis: genetic.
A1-Antitrypsin Deficiency: can cause lung problems and remodeling -> Pulm htn. Same genetic factor that causes COPD.