Interstitial Pulmonary Edema BREAKING POINT Interstitial Pulmonary Edema due to Acute Chronic Ventricular Systolic Failure Definition and Causes Pulmonary edema is defined as an acute and severe left ventricular failure with pulmonary venous hypertension and a large amount of fluid in the lungs (Arnold, 2009 & Arnold, 2008). Precipitating causes differ...
Have you been asked to write a compare and contrast essay? You are not alone. Every year, thousands of students are asked to write compare and contrast essays for their classes in junior high school, high school, and college. Compare and contrast essays are commonly assigned to students...
Interstitial Pulmonary Edema BREAKING POINT Interstitial Pulmonary Edema due to Acute Chronic Ventricular Systolic Failure Definition and Causes Pulmonary edema is defined as an acute and severe left ventricular failure with pulmonary venous hypertension and a large amount of fluid in the lungs (Arnold, 2009 & Arnold, 2008). Precipitating causes differ by age and country, but statistics say that about half of all cases are due to coronary ischemia, decompensation of significant heart failure, arrhythmia and acute volume overload of IV fluids.
Decompensation includes diastolic dysfunction heart failure due, in turn, to hypertension. Drug or dietary non-adherence also often accompanies the condition. With a sudden increase of left ventricular filling pressure, plasma fluid quickly flows into interstitial areas and alveoli from pulmonary capillaries. Pulmonary edema then develops (Arnold & Arnold). Heart failure is in the form of either systolic dysfunction or diastolic dysfunction (Arnold, 2008). In some persons with heart failure, both forms may occur. In the case of systolic dysfunction, heart contractions are less forceful.
The heart is not able to pump as much blood as it normally does. More blood then remains in the lower chambers, and accumulates in the lungs or veins or both. Disorders, which cause systolic dysfunction, damage the whole or part of the heart. The heart, then, becomes unable to contract normally. A combination of the different factors induces a heart failure (Arnold). The most common causes of systolic dysfunction are coronary artery disease, myocarditis, some drugs, heart valve disorders and lung disorders (Arnold, 2009).
Coronary artery disease can injure large parts of the heart muscle by reducing the flow of blood to the heart muscle. This heart muscle needs oxygen for normal contraction. A heart attack can occur when a coronary artery is blocked. This destroys part of the heart muscle and that part ceases to contract normally. An infection can cause myocarditis, or the inflammation of the heart muscle. The infection can damage part or the entire heart muscle and adversely affect its capability to pump blood.
Some drugs used in cancer therapy and some toxins, like alcohol, may also injure heart muscle. Non-steroidal anti-inflammatory drugs, for example, can make the body retain fluid and overwork the heart towards a heart failure. Heart valve disorders impede blood flow through the heart or leak blood backward and can cause heart failure. Stenosis and regurgitation of a heart valve can severely burden the heart until it enlarges and fails to pump properly. An abnormal connection within the chambers leads the blood to circulate within the heart.
This increases workload and lead to heart failure. Disorders such as these can also adversely affect the heart's electrical conduction systems and make it beat faster or irregularly. Abnormal beating disables the heart to pump blood efficiently and heart failure may follow. Lung disorders are further causes of trouble. Some of them can change or injure blood vessels in the lungs. One consequence is that the right side must pump blood harder into the lungs and this can develop cor pulmonale.
In cor pulmonale, the right ventricle enlarges and can lead to right-sided heart failure. Several small blood clots or a single but very large clot can completely block a pulmonary artery and make pumping blood into the pulmonary arteries difficult. A very large clot is immediately fatal (Arnold). Signs and Symptoms Common signs include extreme dyspnea, restlessness and anxiety, blood-tinged sputum, a sense of suffocation, pallor, cyanosis, diaphoresis, frothing at the mouth (Arnold, 2009). Symptoms include rapid pulse and low volume, and varied blood pressure levels.
High blood pressure level suggests substantial cardiac reserve while a systolic blood pressure reading of less than 100 mg/Hg is unfortunate. Strong wheezing, indicative of cardiac asthma, is also probable. Noisy breathing efforts make cardiac auscultation hard. Signs like neck vein distention and peripheral edema may occur and indicate right ventricular failure (Arnold). Diagnosis Interstitial pulmonary edema is diagnosed when clinical evaluation reveals severe dyspnea and pulmonary crackles (Arnold, 2009). Diagnosis is also made by chest x-ray, serum natriuretic peptide or N-terminal-pro BNP, ECG, cardiac markers and other tests for etiology.
In most cases, chest x-ray is immediately performed and establishes the diagnosis with marked interstitial edema. If the diagnosis is inconclusive, bedside measurement of serum BNP levels will help. ECG, pulse oximetry and blood tests are conducted on severely ill patients. An ECG will help identify the cause of the pulmonary edema and direct the choice of treatment. Possible causes of pulmonary edema may be myocardial infarct, valvular dysfunction, hypertensive heart disease, are dilated cardiomyopathy. Severe hypoxemia may also occur.
Retention of CO2 is a late and unfortunate indicator of secondary hypoventilation (Arnold). Treatment This consists in treating the condition, which causes heart failure, lifestyle change, medications, surgery and other interventions (Arnold, 2009). Regimen typically includes oxygen, IV nitrates, diuretics, and morphine. Short-term IV positive inotropes, endotracheal intubation and mechanical ventilation may also be used. Initial treatment oftentimes consists of 100% oxygen by non-rebreather mask in upright position; furosemind; sublingual nitroglycerin; and IV drip.
Additional treatment will depend on etiology, thrombolysis or coronary angioplasty for acute MI or another acute coronary syndrome; an IV vasodilator fir severe hypertension; direct-current cardioversion for tachychardia; and an IB B-blocker, IV digoxin. Other treatments may explore the use of IV BNP and the new intropic drug, levosimendan (Arnold). Prognosis Many people who experience heart failure continue to live for many years (Arnold, 2009). However, 70% of them die of the condition within 10 years.
The severity of the heart failure determines life expectancy if the cause can be corrected and according to the treatment used. About half of all of those with mild heart failure live at least 10 years longer, with severe heart failure live for at least 2 years more. Treatment improves.
The remaining sections cover Conclusions. Subscribe for $1 to unlock the full paper, plus 130,000+ paper examples and the PaperDue AI writing assistant — all included.
Always verify citation format against your institution's current style guide.