PULMONARY EDEMA - CHAPT 23 - PAGE 576 & 839-840

Flash pulmonary edema

A sudden increase in the intravascular pressure in the lung. One example which may occur in the patient who has undergone pneumonectomy, is sometimes termed "flash" pulmonary edema. Hypervolemia is another cause of sudden pulmonary edema.

PULMONARY EDEMA

Abnormal accumulation of fluid in the lung tissue, the alveolar space, or both. It is a Severe, Life-Threatening condition.

Nursing Management of Pulmonary Edema

Assisting w/O2 admin, intubation & mechanical ventilation if respiratory failure occurs. Administer meds & monitor pt response

Assessment and Diagnostics of Pulmonary Edema

Auscultation reveals crackles in the lung bases (*esp. posterior bases) that rapidly progress to the apices of the lungs. These crackles or rales are caused by** the movement of air through the alveolar fluid Chest x-ray reveals increased interstitial markings. Patient may have tachycardia Pulse Oximetry values begin to fall & arterial blood gas analysis demonstrates worsening Hypoxemia

Medical Management of Pulmonary Edema

Focuses on correcting the underlying disorder. If cardiac in origin, then improvement of left ventricular fx is goal. Vasodilators, inotropic medications, afterload or preload agents, or contractility meds may be administered. If problem is fluid overload, diuretics administered and fluids restricted. O2 is administered to correct hypoxemia Intubation and mechanical ventilation may be necessary Patient is extremely anxious, and morphine is prescribed to reduce anxiety and control pain (reduces preload and afterload, decreasing workload)

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Decrease Preload

High doses of loop diuretics such as Furosemide or Torosemide in order to promote large/rapid diuresis VENOUS vasodilators like NTG paste or IV-Tridal to keep blood in periphery, decrease preload and workload of heart Morphine sulfate - (reduces preload and afterload, decreasing workload and relaxes bronchioles to enhance oxygenation)

Cardiac Glycosides

Increase contractility Digoxin like Dobutamine (Dobutrex)-IV critical care inotropic agents Normally, sodium-potassium pumps in the membrane of cells (in this case, cardiac myocytes) pump potassium ions in and sodium ions out. Cardiac glycosides inhibit this pump by stabilizing it in the E2-P transition state, so that sodium cannot be extruded: intracellular sodium concentration therefore increases. A second membrane ion exchanger, NCX, is responsible for 'pumping' calcium ions out of the cell and sodium ions in (3Na/Ca); raised intracellular sodium levels inhibit this pump, so calcium ions are also not extruded and will begin to build up inside the cell, as well. Increased cytoplasmic calcium concentrations cause increased calcium uptake into the sarcoplasmic reticulum via the SERCA2 transporter. Raised calcium stores in the SR allow for greater calcium release on stimulation, so the myocyte can achieve faster and more powerful contraction by cross-bridge cycling. The refractory period of the AV node is increased, so cardiac glycosides also function to regulate heart rate.

Clinical manifestations of pulmonary edema

Increasing respiratory distress, characterized by Dyspnea Air hunger Central Cyanosis Patient usually very anxious and often agitated Foam or froth formed** as fluid leaks into the alveoli and mixes with air Patient experiences acute respiratory distress and may become confused. Symptoms of pulmonary edema may include: •Coughing up (or nurse suctions out) blood or bloody froth •Difficulty breathing when lying down (orthopnea) -- you may notice the need to sleep with your head propped up or use extra pillows •Feeling of "air hunger" or "drowning" (if this feeling wakes you from sleep and causes you to sit up and try to catch your breath, it's called "paroxysmal nocturnal dyspnea") •Grunting, gurgling, or wheezing sounds with breathing •Inability to speak in full sentences because of shortness of breath Other symptoms may include: •Anxiety or restlessness •Decrease in level of alertness (consciousness) •Leg swelling •Pale skin •Sweating (excessive)

Pulmonary Edema Pathophysiology

Most commonly occurs as a result of increased microvascular pressure from abnormal cardiac function. The backup of blood into the pulmonary vasculature resulting from Inadequate Left Ventricular Function causes an increased microvascular pressure, and fluid begins to leak into the interstitial space and the alveoli. Can also be caused by renal failure and other conditions that cause body to retain fluid. Congestive heart failure that leads to pulmonary edema may be caused by: •Heart attack, or any disease of the heart that weakens or stiffens the heart muscle (cardiomyopathy) •Leaking or narrowed heart valves (mitral or aortic valves) •Sudden, severe high blood pressure (hypertension) Pulmonary edema may also be caused by: •Certain medications •High altitude exposure •Kidney failure •Narrowed arteries that bring blood to the kidneys •Lung damaged caused by poisonous gas or severe infection •Major injury

Narcan

Naloxone hydrochloride (Narcan) is kept available and given to the patient who exhibits serious respiratory depression, hypotension and vomiting from Morphine

Decrease afterload

Nitroprusside (Nipride) Vasodilator Nesiritide (Natracore) Natriuretic Peptide

Positioning patient with pulmonary edema

Reduce venous return to the heart by sitting upright, with legs dangling over side of bed. This has the immediate effect of decreasing venous return decreasing right ventricular stroke volume and decreasing lung congestion

Re-expansion pulmonary edema

This may result from a rapid reinflation of the lung after removal of air from a pneumothorax or evacuation of fluid from a large pleural effusion.

Morphine

Use for: Chest pain associated with myocardial infarction=reduces preload and afterload, decreasing workload and relaxes bronchioles to enhance oxygenation) Moderate to severe acute and chronic pain; use w/caution in chronic pain syndromes Pulmonary edema, with or with out associated pain PROMOTES: analgesia, euphoria, and respiratory and physical depression. Secondary pharmacological effects of morphine include depressed responsiveness of alpha-adrenergic receptors (producing peripheral vasodilation) and baroreceptor inhibition. Adverse RX: Hypotension Tachycardia or bradycardia Palpitations Syncope Facial flushing Respiratory depression Euphoria Bronchospasm Dry mouth Allergic reaction