APO - Basic Understanding

APO - Basic Understanding

Pulmonary edema is the accumulation of extravascular fluid in the air sacs or air spaces (alveoli) and parenchyma of the lungs. Abnormal (pathologic) fluid accumulation causes the lungs to become stiff and the air sacs of the lungs to become waterlogged. As a result, breathing becomes very difficult. Acute pulmonary edema is one of the most common life-threatening medical emergencies; intervention is needed as soon as the diagnosis is suspected.

Pulmonary edema is not a disease but a serious complication of another disorder, most commonly congestive heart failure or another cardiac condition such as atherosclerotic heart disease. The edema may be called "cardiogenic pulmonary edema" in these instances. The complication arises when the left side of the heart fails to empty completely with each contraction or has difficulty accepting blood returning from the lungs. As a consequence of this failure, the retained blood creates back pressure, blood and tissue fluid back up, and the vasculature of the lungs becomes congested. The pressure abnormalities are complicated and involve several types of pressure (hydrostatic, intracapillary, interstitial, osmotic, intra- and extravascular pressure), which may vary depending upon the underlying diagnosis or cause of pulmonary edema.

In pulmonary edema associated with heart disorders, the hydrostatic or intravascular pressure continues to rise until fluid is forced out of vessel walls into the alveoli. The pressure also compromises the ability of the lymph system to maintain fluid balance in the lungs, allowing it to build up faster than it can be removed. Changes in pressure interfere with the exchange of oxygen and carbon dioxide (CO2) in the lungs. When the exchange of air and CO2 is abnormal, the imbalance can quickly lead to hypoxia, respiratory arrest, and death.

"Noncardiogenic pulmonary edema" is contingent on an injury to the lung parenchyma or vasculature, and may be secondary to acute lung injury-acute respiratory distress syndrome (ALI- ARDS), lung infections, renal disease, exposure to certain toxins, smoke inhalation, adverse drug reactions, high altitudes, or near drowning.

Points : Occasionally, hoarseness may be present as a result of recurrent laryngeal nerve palsy from mitral stenosis or pulmonary hypertension (Ortner sign).

Causes of acute pulmonary edema divided into :

1. Cardiogenic

• Heart Muscle
• Valvular Disease

2. Non Cardiogenic

3. Neurogenic

AHA ( A.Luisada and L.Cardi ) devides the common causes of acute pulmonary edema into :

• Pulmonary Edema and Arterial Hypertension
• Pulmonary Edema and Coronary Heart Disease
• Pulmonary Edema and Cerebral Diseases
• Pulmonary Edema and Pulmonary Heart Disease
• Pulmonary Edema in Trauma to the Chest
• Pulmonary Edema in Mitral Stenosis
• Pulmonary Edema and Infections
• Pulmonary Edema and Shock

While different duration of clinical signs have led to the another classification of pulmonary

edema , into : 

• Fulminating (5 to 10 minutes)
• Acute (10 to 60 minutes) and 
• Protracted (1 to 36 hours)

Elements Causing Pulmonary Edema.

1. High Pressure in the Pulmonary Capillaries.

This is usually the result of forceful cardiac dynamics. A sudden displacement of blood from the greater to the lesser circulation may favor the edema, especially in the presence of decreased reserve of the left ventricle or mitral block. Severe peripheral vasoconstriction may be caused by epinephrine

(anger, fright, exposure to cold), angiotonin (renal ischemia), or vasomotor stimulation (central lesions, reflex stimulation). This vasoconstriction causes increased arterial resistance resulting in left ventricular strain on the one hand, and increase of venous return to the right heart on the other. This tends, therefore, to produce a high pulmonary capillary pressure through a dual mechanism.

2. Increased Permeability of the Pulmonary

Capillaries. This is favored by increased pulmonary flow (leading to dilatation of the capillaries), allergy, poisons, anoxia, dyspnea (suction effect), chronic heart failure, inhalation of toxic gases. Speculations on whether capillary permeability may be altered by nerve impulses without concomitant changes of capillary pressure have not, as yet, been supported by conclusive evidence. 

3. Decreased Osmotic Pressure of the Blood.

This occurs after prolonged saline infusions, in lipoid nephrosis, starvation or liver diseases.The effect of this factor is widespread. Therefore, either pulmonary edema is part of a diffuse anasarca or is favored by other edematogenic factors.

Classification Of Pulmonary Edema

I. Cardiogenic

Pathophysiology: Caused by rapid transudation of fluid into lungs secondary to increased pulmonary wedge pressure without time for compensation of pulmonary bed. Increased wedge pressure translates to increased pulmonary venous pressure and elevated microvascular pressure, leading to transudation of fluid (Starling’s forces at work!). Can occur at wedge pressures as low as 18mmHg or not until >25mmHg if chronic condition has resulted in increased lymphatic drainage capacity.

Etiology:

A. Heart muscle:

1. Systolic dysfunction: Most common cause of pulmonary edema. Can be due to CAD, HTN,valvular disease, idiopathic dilated cardiomyopathy, toxins, hypothyroidism, viral myocarditis. If condition is somewhat chronic, volume overload is exacerbated by renin-angiotensin system upregulation due to decreased forward flow.
2. Diastolic dysfunction: Increase in ventricular stiffness impairs filling leading to proximal pressure rise. Causes include hypertrophic and restrictive cardiomyopathies, ischemia, HTN crises.

B. Valvular problems:

1.  Mitral stenosis: usually due to rheumatic heart disease.
2.  Aortic stenosis: causes pulmonary edema by requiring elevated LVED filling which translates  to high pulmonary pressures and cardiac ischemia due to impaired diastolic coronary artery  filling.
3. Aortic regurgitation: acutely can be seen in infective endocarditis or aortic dissection.

C. Other:

1. Renal artery stenosis: In some cases, pulmonary edema has been the presenting sign of RAS!
2. Atrial myxoma, intracardiac thrombus impeding left atrial outflow track, congenital membrane in left atrium (cor triatriatum).

II. Noncardiogenic

Definition: Radiographic evidence of alveolar fluid accumulation without elevated pulmonary capillary wedge pressure.

Pathophysiology: Alveolar-capillary membrane becomes damaged and leaky, resulting in movement of proteins and water into interstitial space. Note: hypoalbuminemia does NOT cause pulmonary edema.

Etiologies:

• ARDS (acute respiratory distress syndrome) : Multiple etiologies, including sepsis, DIC, inhaled toxins, radiation pneumonia, inhalation of high oxygen concentrations, severe trauma (thoracic or otherwise). Often occurs within first 2 hours of inciting event but can occur 1-3 days later. Xray shows bilateral alveolar filling pattern. Treat underlying cause. High frequency, low volume ventilation with diuresis proven to be beneficial.
• Reexpansion pulmonary edema : can occur after reexpansion of pneumothorax or following removal of large amounts of pleural fluid (>1.0-1.5 L). Can see within 1 hr in 64%. Ongoing for 24-48hr but symptoms can last up to 5 days. Pathophysiology unknown but worse in patients with chronic collapse.
• High altitude pulmonary edema ( HAPE ) : etiology unclear but thought due to unequal pulmonary vasoconstriction and overperfusion of remaining vessels. Support patient and move to lower altitudes.
• Narcotic overdose : From overdose of heroin or methadone. Usually occurs within 2 hours of injection. Pathophysiology unknown but believed due to direct toxicity, hypoxia, hyperventilation, or cerebral edema. Supportive measure for patient are indicated.
• Pulmonary embolism : Treatment aimed at anticoagulation and supportive measures.
• Kidney failure : In this situation the kidneys do not remove excess fluid and waste products from the body, and the excess fluid accumulates in the lungs
• Inhaled toxins : Inhaled toxins (for example, ammonia or chlorine gas, and smoke inhalation) can cause direct damage to lung tissue.
• Medication side effects : These may occur as a complication of aspirin overdose or with the use of somechemotherapy drug treatments.
• llicit drug use : Non-cardiogenic pulmonary edema is seen in patients who abuse illicit drugs, especially cocaine and heroin.
• Pneumonia : Bacterial or viral pneumonia infections are quite common; however, occasionally become complicated as a collection of fluid develops in the section of the lung that is infected.

III. Neurogenic

Common CNS injuries : epileptic seizures, head injury, cerebral hemorrhage(subarachnoid or

intracerebral). In head injuries, pulmonary edema is seen with elevated intracranial pressures.

Pathophysiology : likely due to sympathetic activation causing pulmonary venoconstriction and increased vascular permeability.

The classification can also be divided according to clinical conditions associated with acute pulmonary edema

A. Cardiovascular disease

1. Syphilitic heart disease (aortic insufficiency; aortitis; aortic aneurysm)
2. Rheumatic heart disease (acute rheumatic carditis; mitral insufficiency; mitral stenosis; aortic insufficiency; aortic stenosis)
3. Coronary heart disease (severe, acute coronary occlusion; minor occlusion plus extensive ischemia or fibrosis of the myocardium)
4. Hypertensive heart disease (pheochromocytoma, essential hypertension; acute glomerulonephritis; hypertensive nephropathies, especially if there is uremia; toxemia of pregnancy)
5. Congenital heart disease (coarctation of the aorta; atrial or ventricular septal defect, patent ductus; Eisenmenger complex; Lutembacher syndrome)
6. Acute or chronic pulmonary heart disease (pulmonary embolism; chronic cor pulmonale)
7. Shock (including that caused by exposure to x-ray radiation)
8. Congestive failure

B. Diseases or lesions of the central nervous system

1. Trauma to the skull
2. Subarachnoid hemorrhage
3. Cerebrovascular attack (hemorrhage, thrombosis, embolism, abscess or tumor)
4. Encephalitis, meningitis, poliomyelitis, tetanus

C. Diseases or lesions of respiratory system

1. Pneumonia, bronchopneumonia (especially influenzal)
2. Drowning, strangulation, asphyxia, respiratory obstruction (edema of the glottis, bronchial asthma, foreign bodies)
3. Inhalation of irritant or toxic gases (including those used in warfare); respiratory burns
4. Following rapid thoracentesis
5. Following trauma to the chest
6. Following lobectomy

D. Allergy

1. Angioneurotic edema

E. Following stimulation of hollow viscera

1. Distention of esophagus, stomach, or gall bladder.
2. Following too rapid emptying of distended bladder or ascites.

F. Surgical and obstetrical cases

1. During pregnancy or after labor (especially, but not only, in cases with rheumatic heart disease, eclampsia, or toxemia)
2. Following transfusions or infusions (especially, but not only, in cardiac or anemic patients)
3. Following surgical manipulation of stellate ganglia.

G. Toxic

1. Following use or overdose of thiourea derivatives, iodides, muscarine, eserine, prostigmine, opium, methyl salicylate, acetic and butyric ether, phenylcarbamide.

H. Miscellaneous

1. Thyroid crises. Beriberi. Insulin shock. Burns.

Management 

Management Goals

Following initial management, medical treatment of Acute Pilmonary Edema focuses on 3 main goals: 

1. reduction of pulmonary venous return (preload reduction), 
2. reduction of systemic vascular resistance (afterload reduction), and, in some cases, 
3. inotropic support. 

Preload reduction decreases pulmonary capillary hydrostatic pressure and reduces fluid transudation into the pulmonary interstitium and alveoli. 

Afterload reduction increases cardiac output and improves renal perfusion, which allows for diuresis in the patient with fluid overload.

Spesific Management 

1. Ventilatory Support 

Noninvasive pressure-support ventilation

Consider noninvasive pressure-support ventilation (NPSV) early when treating patients with severe Acute Pulmonary Edema.  CPAP be the preferred method employed when NPSV is used unless the patient has obstructive airway disease.

2. Preload Reduction

Nitroglycerin (NTG) is the most effective, predictable, and rapidly-acting medication available for preload reduction. Intravenous (IV) NTG at high dosages provides rapid and titratable preload and afterload reduction and is excellent monotherapy for patients with severe Acute Pulmonary Edema. IV NTG can be started with 10mcg/min and then rapidly uptitrated to more than 100mcg/min. The other alternative is NTG given as 3 mg IV boluses every 5 minutes.

Diuretics - Loop diuretics have been considered the cornerstone of Acute Pulmonary Edema treatment for many years. Furosemide is used most commonly. Loop diuretics are presumed to decrease preload through 2 mechanisms: diuresis and direct vasoactivity (venodilation). In most patients, diuresis does not occur for at least 20-90 minutes; therefore, the effect is delayed. Loop diuretics affect the ascending loop of Henle; therefore, the diminished renal perfusion in Acute Pulmonary Edema may delay the onset of effects of loop diuretics.

Morphine sulfate - The use of morphine sulfate in Acute Pulmonary Edema for preload reduction has been commonplace for many years, but good evidence supporting a beneficial hemodynamic effect is lacking. Data suggest that morphine sulfate may contribute to a decrease in cardiac output and that it may be associated with an increased need for ICU admission and endotracheal intubation. Other beneficial hemodynamic effect from morphine is probably due to anxiolysis, with a resulting decrease in catecholamine production and a decrease in systemic vascular resistance.

3. Afterload Reduction

ACE inhibitors are generally considered the cornerstones for treating chronic CHF, and studies have demonstrated excellent results with ACE inhibitors for the treatment of acute decompensated CHF and Acute Pulmonary Edema. The use of ACE inhibitors in Acute Pulmonary Edema is associated with reduced admission rates to ICUs and decreased endotracheal intubation rates and length of ICU stay.

The hemodynamic effects of ACE inhibitors include reduced afterload, improved stroke volume and cardiac output, and a slight reduction in preload. The last effects happen when renal perfusion improves after cardiac output improves and diuresis occurs.

Enalapril 1.25 mg IV Captopril 25 mg, given sublingually, result in hemodynamic and subjective improvements within 10 minutes. Improvements occur much more slowly with the oral route.

Angiotensin II receptor blockers (ARBs) have comparable beneficial effects in heart failure. Studies have proposed a role for ACE inhibitors and ARBs in preventing structural and electrical remodeling of the heart, resulting in a reduced incidence of arrhythmias.

The Valsartan Heart Failure Trial (Val-HeFT) showed that Valsartan reduces the incidence of atrial fibrillation (AF) by 37%. (BNP level and advanced age were the strongest independent predictors for AF occurrence.)  Similarly, the Candesartan in Heart Failure: Assessment in Reduction of Mortality and Morbidity (CHARM) trial showed a reduction in the onset of AF in patients who were treated with Candesartan compared with placebo, with a median follow-up period of 37.7 months.

Nitroprusside results in simultaneous preload and afterload reduction by causing direct smooth-muscle relaxation, with an increased effect on afterload. Afterload reduction is associated with increased cardiac output. The potency and rapidity of onset and offset of effect make this an ideal medication for patients who are critically ill. It may induce precipitous falls and labile fluctuations in blood pressure; intra-arterial blood pressure monitoring is often recommended.

Nitroprusside should generally be avoided in the setting of acute MI. Its use is associated with the shunting of blood away from ischemic myocardium toward healthy myocardium (ie, coronary steal syndrome), which potentiates ischemia.

If Nitroprusside is used, convert therapy to oral or alternative IV vasodilator therapy as soon as possible because prolonged use is associated with thiocyanate toxicity. Use in pregnancy is associated with fetal thiocyanate toxicity. Prolonged infusion can induce tolerance, and reflex tachycardia may occur.

4. Catecholamines 

Inotropic support is usually used when preload- and afterload-reduction strategies are not successful or when hypotension precludes the use of these strategies. Two main classes of inotropic agents are available: catecholamine agents and phosphodiesterase inhibitors (PDIs). Calcium-sensitizer agents are a new class of medications that have notably beneficial effects in acute decompensated heart failure; these drugs are under investigation.

A. Dobutamine

Dobutamine, a catecholamine agent, mainly serves as a beta1-receptor agonist, though it has some beta2-receptor and minimal alpha-receptor activity. IV dobutamine induces significant positive inotropic effects, with mild chronotropic effects. It also induces mild peripheral vasodilation (decrease in afterload). The combination effect of increased inotropy with decreased afterload significantly increases cardiac output. Combination use with IV NTG may be ideal for patients with MI and Acute Pulmonary Edema and mild hypotension to simultaneously reduce preload and increase cardiac output. In general, avoid dobutamine in patients with moderate or severe hypotension (eg, systolic BP < 80 mm Hg), because of the peripheral vasodilation.

B. Dopamine

The vascular and myocardial receptor effects of dopamine, a catecholamine agent, are dose dependent. Low dosages of 0.5-5 mcg/kg/min stimulate dopaminergic receptors in the renal and splanchnic vascular beds, causing vasodilation and increasing diuresis. Moderate dosages of 5-10 mcg/kg/min stimulate beta-receptors in the myocardium, increasing cardiac contractility and heart rate.

High dosages of 15-20 mcg/kg/min stimulate alpha-receptors, resulting in peripheral vasoconstriction (increased afterload), increased blood pressure, and no further improvement in cardiac output.

Moderate and high dosages are arrhythmogenic and increase myocardial oxygen demand (with the potential for myocardial ischemia). Therefore, use these dosages only in patients with Acute Pulmonary Edema who cannot tolerate dobutamine because of severe hypotension (eg, systolic blood pressure 60-80 mm Hg)

C. Norepinephrine

Norepinephrine, a catecholamine agent, primarily stimulates alpha receptors, significantly increasing afterload (and the potential for myocardial ischemia) and reducing cardiac output. Norepinephrine is generally reserved for patients with profound hypotension (eg, systolic blood pressure < 60 mm Hg). After blood pressure is restored, add other medications to maintain cardiac output.

5. Ultrafiltration

Ultrafiltration (UF) is a method of fluid removal that is particularly useful in patients with renal dysfunction and expected diuretic resistance.

The randomized Ultrafiltration Versus Intravenous Diuretics for Patients Hospitalized for Acute Decompensated Heart Failure (UNLOAD) trial demonstrated that ultrafiltration was superior to the use of IV diuretics in controlling net fluid loss and rehospitalization in hypervolemic patients with heart failure. These results indicated that UF should be considered in patients with volume overload and acute CHF who have not responded well to moderate to large doses of diuretic treatment or in whom the adverse effects of such treatment (eg, renal dysfunction) do not allow initiation or continuation of the therapy. Broader application of UF needs further investigation with larger clinical trials to determine the efficacy and safety of this method.

Points :

1. Elevation of pulmonary wedge pressures helps to differentiate cardiogenic from non-cardiogenic causes of pulmonary edema.
2. CXR, ECG, and ABG are indicated in most patients. History and physical exam can help differentiate causes.
3. For treatment think: L-M-N-O-P (Lasix-Morphine-Nitro-Oxygen-Position/Positive pressure ventilation)

Source : www.medicine.ucsf.edu

             www.emedicinehealth.com

             www.circ.ahajournals.org

             www.emedicine.medscape.com