Hospital-acquired pneumonia Hospital-acquired pneumonia is an infection of the lungs that occurs during a hospital stay.

Causes Pneumonia is a very common illness. It is caused by many different germs, and the infection can range in seriousness from mild to lifethreatening. Hospital-acquired pneumonia tends to be more serious than other lung infections, because: Patients in the hospital are often sicker and unable to fight off germs. The types of germs present in a hospital are often more dangerous than those encountered in the community. Hospital-acquired pneumonia occurs more often in patients who are using a respirator machine (also called a ventilator) to help them breathe. When pneumonia occurs in a patient who is on a ventilator, it is known as ventilator-associated pneumonia. Risk factors for hospital-acquired pneumonia include: Alcoholism

bacteria in each hospital -- Staphylococcus aureus and gramnegative bacteria. Supportive treatment includes: Oxygen Lung treatments to loosen and remove thick mucus from the lungs Pathophysiology The pathophysiology of hypertensive heart disease is a complex interplay of various hemodynamic, structural, neuroendocrine, cellular, and molecular factors. These factors play integral roles in the development of hypertensionand its complications; however, elevated BP itself can modulate these factors. Elevated BP leads to adverse changes in cardiac structure and function in 2 ways: directly, by increased afterload, and indirectly, by associated neurohormonal and vascular changes. Elevated 24-hour ambulatory BP and nocturnal BP have been demonstrated to be more closely related to various cardiac pathologies, especially in black persons. The pathophysiologies of the various cardiac effects of hypertension differ and are described in this section. Left ventricular hypertrophy Of patients with hypertension, 15-20% develops LVH. The risk of LVH is increased 2-fold by associated obesity. The prevalence of LVH based on electrocardiogram (ECG) findings, which are not a sensitive marker at the time of diagnosis of hypertension, is variable. [1, 2] Studies have shown a direct relationship between the level and duration of elevated BP and LVH. LVH, defined as an increase in the mass of the left ventricle (LV), is caused by the response of myocytes to various stimuli accompanying elevated BP. Myocyte hypertrophy can occur as a compensatory response to increased afterload. Mechanical and neurohormonal stimuli accompanying hypertension can lead to activation of myocardial cell growth, gene expression (of which some occurs primarily in fetal cardiomyocytes), and, thus, to LVH. In addition, activation of the renin-angiotensin system, through the action of angiotensin II on angiotensin I receptors, leads to growth of interstitium and cell matrix components. In summary, the development of LVH is characterized by myocyte hypertrophy and by an imbalance between the myocytes and the interstitium of the myocardial skeletal structure. Various patterns of LVH have been described, including concentric remodeling, concentric LVH, and eccentric LVH. Concentric LVH is an increase in LV thickness and LV mass with increased LV diastolic pressure and volume, commonly observed in persons with hypertension; this is a marker of poor prognosis in these patients. Compare concentric LVH with eccentric LVH, in which LV thickness is increased not uniformly but at certain sites, such as the septum. Although the development of LVH initially plays a protective role in response to increased wall stress to maintain adequate cardiac output, it later leads to the development of diastolic and, ultimately, systolic myocardial dysfunction. Interestingly, findings from a prospective study (The Multiethnic Study of Atherosclerosis [MESA] trial) also indicate a higher risk of developing systemic hypertension among patients in the higher quartiles of the LV mass at baseline. Left atrial abnormalities Frequently underappreciated, structural and functional changes of the left atrium (LA) are very common in patients with hypertension. The increased afterload imposed on the LA by the elevated LV enddiastolic pressure secondary to increased BP leads to impairment of the LA and LA appendage function plus increased LA size and thickness. Increased LA size accompanying hypertension in the absence of valvular heart disease or systolic dysfunction usually implies chronicity of hypertension and may correlate with the severity of LV diastolic dysfunction. In addition to these structural changes, these patients are predisposed to atrial fibrillation. Atrial fibrillation, with loss of atrial contribution in the presence of diastolic dysfunction, may precipitate overt heart failure. Valvular disease Although valvular disease does not cause hypertensive heart disease, chronic and severe hypertension can cause aortic root dilatation, leading to significant aortic insufficiency. Some degree of hemodynamically insignificant aortic insufficiency is often found in patients with uncontrolled hypertension. An acute rise in BP may accentuate the degree of aortic insufficiency, with return to baseline

Recent illness Symptoms Cough that may produce mucus-like, greenish, or pus-like phlegm (sputum) Chills

Being on a breathing machine Breathing saliva or food into the lungs (aspiration) Chest surgery Immunosuppression (immune system does not work well) Long-term (chronic) lung disease Not being fully alert Older age

Sharp or stabbing chest pain that gets worse with deep breathing or coughing Shortness of breath Exams and Tests A physical examination shows: Crackles or decreased breath sounds when listening to the chest with a stethoscope Decreased oxygen

Easy fatigue Excessive sweating (rare) Fever General discomfort, uneasiness, or ill feeling (malaise) Headache Joint stiffness and pain (rare) Loss of appetite Muscle stiffness (rare) Nausea and vomiting

Respiratory distress Tests performed may include: Arterial blood gases

Blood cultures

Chest x-ray or CT scan Complete blood count (CBC) Sputum culture

Sputum gram stain Treatment Treatment aims to cure the infection with antibiotics. An antibiotic is chosen based on the specific germ found by sputum culture. However, the bacteria cannot always be identified with tests. Antibiotic therapy is given to fight the most common bacteria that infect hospitalized patients, taking into account the most common

when the BP is better controlled. In addition to causingaortic regurgitation, hypertension is also thought to accelerate the process of aortic sclerosis and cause mitral regurgitation. Heart failure Heart failure is a common complication of chronically elevated BP. Patients with hypertension are either asymptomatic but at risk of developing of heart failure (stage A or B per American College of Cardiology [ACC] / American Heart Association [AHA] classification depending upon if they have developed structural heart disease as a consequence of hypertension) or have symptomatic heart failure (stage C or D per ACC/AHA classification). Hypertension as a cause of CHF is frequently underrecognized, partly because at the time heart failure develops, the dysfunctioning LV is unable to generate the high BP, thus obscuring the etiology of the heart failure. The prevalence of asymptomatic diastolic dysfunction in patients with hypertension and without LVH may be as high as 33%. Chronically elevated afterload and the resulting LVH can adversely affect both the active early relaxation phase and late compliance phase of ventricular diastole. Diastolic dysfunction is common in persons with hypertension. It is often, but not invariably, accompanied by LVH. In addition to elevated afterload, other factors that may contribute to the development of diastolic dysfunction include coexistent coronary artery disease, aging, systolic dysfunction, and structural abnormalities such as fibrosis and LVH. Asymptomatic systolic dysfunction usually follows. Later in the course of disease, the LVH fails to compensate by increasing cardiac output in the face of elevated BP, and the left ventricular cavity begins to dilate to maintain cardiac output. As the disease enters the end stage, LV systolic function decreases further. This leads to further increases in activation of the neurohormonal and renin-angiotensin systems, leading to increases in salt and water retention and increased peripheral vasoconstriction, eventually overwhelming the already compromised LV and progressing to the stage of symptomatic systolic dysfunction. Apoptosis, or programmed cell death, stimulated by myocyte hypertrophy and the imbalance between its stimulants and inhibitors, is considered to play an important part in the transition from compensated to decompensated stage. The patient may become symptomatic during the asymptomatic stages of the LV systolic or diastolic dysfunction, owing to changes in afterload conditions or to the presence of other insults to the myocardium (eg, ischemia, infarction). A sudden increase in BP can lead to acute pulmonary edema without necessarily changing the LV ejection fraction.[3]Generally, development of asymptomatic or symptomatic LV dilatation or dysfunction heralds rapid deterioration in clinical status and a markedly increased risk of death. In addition to LV dysfunction, right ventricular thickening and diastolic dysfunction also develop as results of septal thickening and LV dysfunction. Myocardial ischemia Patients with angina have a high prevalence of hypertension. Hypertension is an established risk factor for the development of coronary artery disease, almost doubling the risk. The development of ischemia in patients with hypertension is multifactorial. Importantly, in patients with hypertension, angina can occur in the absence of epicardial coronary artery disease. The reason is 2-fold. Increased afterload secondary to hypertension leads to an increase in LV wall tension and transmural pressure, compromising coronary blood flow during diastole. In addition, the microvasculature, beyond the epicardial coronary arteries, has been shown to be dysfunctional in patients with hypertension, and it may be unable to compensate for increased metabolic and oxygen demand. The development and progression of arteriosclerosis, the hallmark of coronary artery disease, is exacerbated in arteries subjected to chronically elevated BP. Shear stress associated with hypertension and the resulting endothelial dysfunction cause impairment in the synthesis and release of the potent vasodilator nitric oxide. A decreased nitric oxide level promotes the development and acceleration of arteriosclerosis and plaque formation. Morphologic features of the plaque are identical to those observed in patients without hypertension. Cardiac arrhythmias Cardiac arrhythmias commonly observed in patients with hypertension include atrial fibrillation, premature ventricular contractions (PVCs), andventricular tachycardia (VT).[4]

The risk of sudden cardiac death is increased.[5] Various mechanisms thought to play a part in the pathogenesis of arrhythmias include altered cellular structure and metabolism, inhomogeneity of the myocardium, poor perfusion, myocardial fibrosis, and fluctuation in afterload. All of these may lead to an increased risk of ventricular tachyarrhythmias. Atrial fibrillation (paroxysmal, chronic recurrent, or chronic persistent) is observed frequently in patients with hypertension.[6] In fact, elevated BP is the most common cause of atrial fibrillation in the Western hemisphere. In one study, nearly 50% of patients with atrial fibrillation had hypertension. Although the exact etiology is not known, left atrial structural abnormalities, associated coronary artery disease, and LVH have been suggested as possible contributing factors. The development of atrial fibrillation can cause decompensation of systolic and, more importantly, diastolic dysfunction, owing to loss of atrial kick, and it also increases the risk of thromboembolic complications, most notably stroke. Premature ventricular contractions, ventricular arrhythmias, and sudden cardiac death are observed more often in patients with LVH than in those without LVH. The etiology of these arrhythmias is thought to be concomitant coronary artery disease and myocardial fibrosis. Symptoms Symptoms of hypertensive heart disease depend on the duration, severity, and type of disease. In addition, the patient may or may not be aware of the presence of hypertension, which is why hypertension has been named "the silent killer." Left ventricular hypertrophy Patients with LVH alone are totally asymptomatic, unless the LVH leads to the development of diastolic dysfunction and heart failure. Heart failure Although symptomatic diastolic heart failure and systolic heart failure are indistinguishable, the clinical history may be quite revealing. In particular, individuals who abruptly develop severe symptoms of CHF and rapidly return to baseline with medical therapy are more likely to have isolated diastolic dysfunction. Heart failure symptoms include exertional and nonexertional dyspnea (New York Heart Association [NYHA] classes I-IV); orthopnea; paroxysmal nocturnal dyspnea; fatigue (more common in systolic dysfunction); ankle edema and weight gain; abdominal pain secondary to a congested, distended liver; and in severe cases, altered mentation. Patients can present with acute pulmonary edema due to sudden decompensation in LV systolic or diastolic dysfunction caused by precipitating factors such as acute rise in BP, dietary indiscretion, or myocardial ischemia. Patients can develop cardiac arrhythmias, especially atrial fibrillation, or they can develop symptoms of heart failure insidiously over time. Myocardial ischemia Angina, a frequent complication of hypertensive heart disease, is also indistinguishable from other causes of myocardial ischemia. Typical symptoms of angina include substernal chest pain lasting less than 15 minutes (vs >20 min in infarction). Pain is often described as a heaviness, pressure, and/or squeezing; radiating to the neck, jaw, upper back, or left arm; provoked by emotional or physical exertion; and relieved with rest or sublingual nitroglycerin. However, patients may also present with atypical symptoms without chest pain, such as exertional dyspnea or excessive fatigue, commonly referred to as an angina equivalent. Female patients, in particular, are more likely to present atypically. Patients may present with chronic stable angina or acute coronary syndrome, including myocardial infarction without ST-segment elevation and acute myocardial infarction with ST elevation. Ischemic ECG changes may be found in individuals presenting with hypertensive crisis in whom no significant coronary atherosclerosis is detectable by coronary angiography. Acute coronary symptoms can be precipitated by a ruptured atherosclerotic plaque or by an acute and severe rise in BP leading to a sudden increase in transmural pressure without a change in stability of the plaque. Cardiac arrhythmias Irregular or abnormal heart rhythms can cause a variety of symptoms, including palpitations, near or total syncope, precipitation of angina, sudden cardiac death, and precipitation of heart failure, especially with atrial fibrillation in diastolic dysfunction.

Diagnostic Overview The following conditions should also be considered when evaluating hypertensive heart disease: Coronary artery atherosclerosis

Sleep apnea Intraventricular Hemorrhage Intraventricular Hemorrhage What is intraventricular hemorrhage (IVH)? Intraventricular hemorrhage (IVH) is bleeding inside or around the ventricles, the spaces in the brain containing the cerebral spinal fluid. "intraventricular" means within the ventricles

Hypertrophic cardiomyopathy Athlete's heart (with LVH) Congestive heart failure due to other etiologies Atrial fibrillation due to other etiologies Diastolic dysfunction due to other etiologies

Grade 4 - bleeding into the brain tissues around the ventricles. Grades 1 and 2 are most common, and often there are no further complications. Grades 3 and 4 are the most serious and may result in long-term brain injury to the baby. Hydrocephalus (too much cerebral spinal fluid in the brain) may develop after severe IVH. What are the symptoms of intraventricular hemorrhage? The following are the most common symptoms of intraventricular hemorrhage (IVH). However, each baby may experience symptoms differently. Symptoms may include: apnea and bradycardia (stopping breathing and low heart rate) pale or blue coloring (cyanosis)

Grade 3 - ventricles are enlarged by the blood.

"hemorrhage" means excessive bleeding Intraventricular hemorrhage is most common in premature babies, especially very low birthweight babies weighing less than 1,500 grams (3 pounds, 4 ounces). What causes intraventricular hemorrhage? It is not clear why IVH occurs. Bleeding can occur because blood vessels in a premature baby's brain are very fragile and immature and easily rupture. Babies with respiratory problems such as hyaline membrane disease, or other complications of prematurity, are more likely to have IVH. The smaller and more premature the baby, the more likely IVH will occur. Nearly all IVH occurs within the first three days of life. Why is intraventricular hemorrhage a concern? Bleeding in the brain can put pressure on the nerve cells and damage them. Severe damage to cells can lead to brain injury. What are the different grades of intraventricular hemorrhage? The amount of bleeding varies. IVH is often described in four grades: Grade 1 - bleeding occurs just in a small area of the ventricles. Grade 2 - bleeding also occurs inside the ventricles.

swelling or bulging of the fontanelles, the "soft spots" between the bones of the baby's head anemia (low blood count) The symptoms of IVH may resemble other conditions or medical problems. Always consult your baby's physician for a diagnosis. How is intraventricular hemorrhage diagnosed? In addition to a complete medical history and a physical examination, a cranial (head) ultrasound is usually used to diagnose IVH. This test uses sound waves to create a picture of internal structures. A cranial ultrasound can view the inside of the baby's brain through the fontanelles, the spaces between the bones of the baby's head. With the ultrasound, the amount of bleeding can be graded. Treatment for intraventricular hemorrhage: There is no specific treatment for IVH, except to treat any other health problems that may worsen the condition. Although care of sick and premature babies has advanced greatly, it is not possible to prevent IVH from occurring. However, giving the mother medications (called corticosteroids) before delivery has been shown to lower the risk of IVH in the baby. These steroids are often given to women between 24 and 34 weeks gestation who are at risk of early delivery.

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