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INSULIN Insulin is a naturally occurring hormone secreted by the pancreas.

Many people with diabetes are prescribed insulin, either because their bodies do not produce insulin (type 1 diabetes) or do not use insulin properly (type 2 diabetes). There are more than 20 types of insulin sold in the United States. These insulins differ in how they are made, how they work in the body, and how much they cost. Your doctor will help you find the right type of insulin for your health needs and your lifestyle.

Insulin has 3 characteristics:

Onset is the length of time before insulin reaches the bloodstream and begins lowering blood glucose. Peaktime is the time during which insulin is at maximum strength in terms of lowering blood glucose. Duration is how long insulin continues to lower blood glucose.

Insulin Strength All insulins come dissolved or suspended in liquids. The standard and most commonly used

There are different types of insulin depending on how quickly they work, when they peak, and how long they last. Insulin is available in different strengths; the most common is U-100. All insulin available in the United States is manufactured in a laboratory, but animal insulin can still be imported for personal use.

strength in the United States today is U-100, which means it has 100 units of insulin per milliliter of fluid, though U-500 insulin is available for patients who are extremely insulin resistant. U-40, which has 40 units of insulin per milliliter of fluid, has generally been phased out around the world, but it is possible that it could still be found in some places (and U-40 insulin is still used in veterinary care). If you're traveling outside of the U.S., be certain to match your insulin strength with the correct size syringe. Insulin Additives All insulins have added ingredients. These prevent bacteria from growing and help maintain a neutral balance between acids and bases. In addition, intermediate and long-acting insulins also contain ingredients that prolong their actions. In some rare cases, the additives can bring on an allergic reaction.

Inside the pancreas, beta cells make the hormone insulin. With each meal, beta cells release insulin to help the body use or store the blood glucose it gets from food. In people with type 1 diabetes, the pancreas no longer makes insulin. The beta cells have been destroyed and they need insulin shots to use glucose from meals. People with type 2 diabetes make insulin, but their bodies don't respond well to it. Some people with type 2 diabetes need diabetes pills or insulin shots to help their bodies use glucose for energy. Insulin cannot be taken as a pill because it would be broken down during digestion just like the protein in food. It must be injected into the fat under your skin for it to get into your blood. Types of Insulin

Rapid-acting insulin, begins to work about 15 minutes after injection, peaks in about 1 hour, and continues to work for 2 to 4 hours. Types: Insulin glulisine (Apidra), insulin lispro (Humalog), and insulin aspart (NovoLog) Regular or Short-acting insulin usually reaches the bloodstream within 30 minutes after injection, peaks anywhere from 2 to 3 hours after injection, and is effective for approximately 3 to 6 hours. Types: Humulin R, Novolin R Intermediate-acting insulin generally reaches the bloodstream about 2 to 4 hours after injection, peaks 4 to 12 hours later, and is effective for about 12 to 18 hours. Types: NPH (Humulin N, Novolin N) Long-acting insulin reaches the bloodstream several hours after injection and tends to lower glucose levels fairly evenly over a 24-hour period. Types: Insulin detemir (Levemir) and insulin glargine (Lantus)

ROUTES

Insulin is required for people with type 1 diabetes and sometimes necessary for people with type 2 diabetes. Syringe is the most common form of insulin delivery, but there are other options, including insulin pens and pumps. Insulin should be injected in the same general area of the body for consistency, but not the exact same place. Insulin delivery should be timed with meals to effectively process the glucose entering your system.

Insulin Therapy With the help of your health care team, you can find an insulin routine that will keep your blood glucose near normal, help you feel good, and fit your lifestyle. Type 1

Premixed insulin can be helpful for people who have trouble drawing up insulin out of two bottles and reading the correct directions and dosages. It is also useful for those who have poor eyesight or dexterity and is convenient for people whose diabetes has been stabilized on this combination. Characteristics of Insulin

People diagnosed with type 1 diabetes usually start with two injections of insulin per day of two different types of insulin and generally progress to three or four injections per day of insulin of different types. The types of insulin used depend on their blood glucose levels. Studies have shown that three or four injections of insulin a day give the best blood glucose control and can prevent or delay the eye, kidney, and nerve damage caused by diabetes. Type 2 Most people with type 2 diabetes may need one injection per day without any diabetes pills. Some may need a single injection of insulin in the evening (at supper or bedtime) along with diabetes pills. Sometimes diabetes pills stop working, and people with type 2 diabetes will start with two injections per day of two different types of insulin. They may progress to three or four injections of insulin per day. Fine-Tuning Your Blood Glucose Many factors affect your blood glucose levels, including the following:

Pump Therapy Insulin pumps help you manage diabetes by delivering insulin 24 hours a day through a catheter placed under the skin. Read more about insulin pumps. Site Rotation The place on your body where you inject insulin affects your blood glucose level. Insulin enters the blood at different speeds when injected at different sites. Insulin shots work fastest when given in the abdomen. Insulin arrives in the blood a little more slowly from the upper arms and even more slowly from the thighs and buttocks. Injecting insulin in the same general area (for example, your abdomen) will give you the best results from your insulin. This is because the insulin will reach the blood with about the same speed with each insulin shot. Don't inject the insulin in exactly the same place each time, but move around the same area. Each mealtime injection of insulin should be given in the same general area for best results. For example, giving your before-breakfast insulin injection in the abdomen and your before-supper insulin injection in the leg each day give more similar blood glucose results. If you inject insulin near the same place each time, hard lumps or extra fatty deposits may develop. Both of these problems are unsightly and make the insulin action less reliable. Ask your health care provider if you aren't sure where to inject your insulin. Timing Insulin shots are most effective when you take them so that insulin goes to work when glucose from your food starts to enter your blood. For example, regular insulin works best if you take it 30 minutes before you eat. Too much insulin or not enough? High morning blood glucose levels before breakfast can be a puzzle. If you haven't eaten, why did your blood glucose level go up? There are two common reasons for high before-breakfast blood glucose levels. One relates to hormones that are released in the early part of sleep [called the Dawn Phenomenon - the early-morning (4 a.m. to 8 a.m.) rise in blood glucose level.]. The other is from taking too little insulin in the evening. To see which one is the cause, set your alarm to self-monitor around 2 or 3 a.m. for several nights and discuss the results with your health care provider.

What you eat How much and when you exercise Where you inject your insulin When you take your insulin injections Illness Stress

Self Monitoring Checking your blood glucose and looking over results can help you understand how exercise, an exciting event, or different foods affect your blood glucose level. You can use it to predict and avoid low or high blood glucose levels. You can also use this information to make decisions about your insulin dose, food, and activity. For more information, see our Blood Glucose Control section. Insulin Delivery Many people who take insulin use a syringe, but there are other options as well. Insulin Pens Some insulin pens contain a cartridge of insulin that is inserted into the pen and some are pre-filled with insulin and discarded after all the insulin has been used. The insulin dose is dialed on the pen, and the insulin is injected through a needle, much like using a syringe. Cartridges and pre-filled insulin pens only contain one type of insulin. Two injections must be given with an insulin pen if using two types of insulin.

ACUTE RESPIRATORY FAILURE Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic or hypercapnic. Hypoxemic respiratory failure (type I) is characterized by an arterial oxygen tension (P a O2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (P a CO2). This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage. Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and chronic obstructive pulmonary disease [COPD]). Respiratory failure may be further classified as either acute or chronic. Although acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent. Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3. Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased. The distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases. The clinical markers of chronic hypoxemia, such as polycythemia or cor pulmonale, suggest a long-standing disorder. Arterial blood gases should be evaluated in all patients who are seriously ill or in whom respiratory failure is suspected. Chest radiography is essential. Echocardiography is not routine but is sometimes useful. Pulmonary functions tests (PFTs) may be helpful. Electrocardiography (ECG) should be performed to assess the possibility of a cardiovascular cause of respiratory failure; it also may detect dysrhythmias resulting from severe hypoxemia or acidosis. Right-heart catheterization is controversial (see Workup). Hypoxemia is the major immediate threat to organ function. After the patients hypoxemia is corrected and the ventilatory and hemodynamic status have stabilized, every attempt should be made to identify and correct the underlying pathophysiologic process that led to respiratory failure in the first place. The specific treatment depends on the etiology of respiratory failure.

respiratory muscles, and chest wall. Patients who have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shock often present with respiratory failure. Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue. Ventilatory demand is the spontaneous minute ventilation that results in a stable Pa CO2. Normally, ventilatory capacity greatly exceeds ventilatory demand. Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller. Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing. Respiratory physiology The act of respiration engages 3 processes:

Transfer of oxygen across the alveolus Transport of oxygen to the tissues Removal of carbon dioxide from blood into the alveolus and then into the environment Respiratory failure may occur from malfunctioning of any of these processes. In order to understand the pathophysiologic basis of acute respiratory failure, an understanding of pulmonary gas exchange is essential. Gas exchange Respiration primarily occurs at the alveolar capillary units of the lungs, where exchange of oxygen and carbon dioxide between alveolar gas and blood takes place. After diffusing into the blood, the oxygen molecules reversibly bind to the hemoglobin. Each molecule of hemoglobin contains 4 sites for combination with molecular oxygen; 1 g of hemoglobin combines with a maximum of 1.36 mL of oxygen. The quantity of oxygen combined with hemoglobin depends on the level of blood P a O2. This relationship, expressed as the oxygen hemoglobin dissociation curve, is not linear but has a sigmoid-shaped curve with a steep slope between a Pa O2of 10 and 50 mm Hg and a flat portion above a Pa O2 of 70 mm Hg. The carbon dioxide is transported in 3 main forms: (1) in simple solution, (2) as bicarbonate, and (3) combined with protein of hemoglobin as a carbamino compound. During ideal gas exchange, blood flow and ventilation would perfectly match each other, resulting in no alveolar-arterial oxygen tension (PO2) gradient. However, even in normal lungs, not all alveoli are ventilated and perfused perfectly. For a given perfusion, some alveoli are underventilated, while others are overventilated. Similarly, for known alveolar ventilation, some units are underperfused, while others are overperfused. The optimally ventilated alveoli that are not perfused well have a large ventilation-to-perfusion ratio (V/Q) and are called high-V/Q units (which act like dead space). Alveoli that are optimally perfused but not adequately ventilated are called low-V/Q units (which act like a shunt). Alveolar ventilation

PATHOPHYSIOLOGY Respiratory failure can arise from an abnormality in any of the components of the respiratory system, including the airways, alveoli, central nervous system (CNS), peripheral nervous system,

At steady state, the rate of carbon dioxide production by the tissues is constant and equals the rate of carbon dioxide elimination by the lung. This relation is expressed by the following equation: VA = K VCO2/ Pa CO2 where K is a constant (0.863), VA is alveolar ventilation, and VCO2 is carbon dioxide ventilation. This relation determines whether the alveolar ventilation is adequate for metabolic needs of the body. The efficiency of lungs at carrying out of respiration can be further evaluated by measuring the alveolar-arterial PO2 gradient. This difference is calculated by the following equation: PA O2 = FI O2 (PB PH2 O) PA CO2/R where PA O2 is alveolar PO2, FI O2 is fractional concentration of oxygen in inspired gas, P B is barometric pressure, PH2 O is water vapor pressure at 37C, PA CO2 is alveolar PCO2 (assumed to be equal to Pa CO2), and R is respiratory exchange ratio. R depends on oxygen consumption and carbon dioxide production. At rest, the ratio of VCO2 to oxygen ventilation (VO2) is approximately 0.8. Even normal lungs have some degree of V/Q mismatching and a small quantity of right-to-left shunt, with PA O2 slightly higher than Pa O2. However, an increase in the alveolar-arterial PO2 gradient above 15-20 mm Hg indicates pulmonary disease as the cause of hypoxemia. Hypoxemic respiratory failure The pathophysiologic mechanisms that account for the hypoxemia observed in a wide variety of diseases are V/Q mismatch and shunt. These 2 mechanisms lead to widening of the alveolararterial PO2 gradient, which normally is less than 15 mm Hg. They can be differentiated by assessing the response to oxygen supplementation or calculating the shunt fraction after inhalation of 100% oxygen. In most patients with hypoxemic respiratory failure, these 2 mechanisms coexist. V/Q mismatch V/Q mismatch is the most common cause of hypoxemia. Alveolar units may vary from low-V/Q to high-V/Q in the presence of a disease process. The low-V/Q units contribute to hypoxemia and hypercapnia, whereas the high-V/Q units waste ventilation but do not affect gas exchange unless the abnormality is quite severe. The low V/Q ratio may occur either from a decrease in ventilation secondary to airway or interstitial lung disease or from overperfusion in the presence of normal ventilation. The overperfusion may occur in case of pulmonary embolism, where the blood is diverted to normally ventilated units from regions of lungs that have blood flow obstruction secondary to embolism. Administration of 100% oxygen eliminates all of the low-V/Q units, thus leading to correction of hypoxemia. Hypoxemia increases minute ventilation by chemoreceptor stimulation, but the Pa CO2 generally is not affected. Shunt Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The deoxygenated blood (mixed venous blood) bypasses the ventilated alveoli and mixes with

oxygenated blood that has flowed through the ventilated alveoli, consequently leading to a reduction in arterial blood content. The shunt is calculated by the following equation: QS/QT = (CC O2 Ca O2)/CC O2 Cv O2) where QS/QT is the shunt fraction, CC O2 is capillary oxygen content (calculated from ideal PA O2), Ca O2 is arterial oxygen content (derived from Pa O2 by using the oxygen dissociation curve), and Cv O2 is mixed venous oxygen content (assumed or measured by drawing mixed venous blood from a pulmonary arterial catheter). Anatomic shunt exists in normal lungs because of the bronchial and thebesian circulations, which account for 2-3% of shunt. A normal right-to-left shunt may occur from atrial septal defect, ventricular septal defect, patent ductus arteriosus, or arteriovenous malformation in the lung. Shunt as a cause of hypoxemia is observed primarily in pneumonia, atelectasis, and severe pulmonary edema of either cardiac or noncardiac origin. Hypercapnia generally does not develop unless the shunt is excessive (> 60%). Compared with V/Q mismatch, hypoxemia produced by shunt is difficult to correct by means of oxygen administration. Hypercapnic respiratory failure At a constant rate of carbon dioxide production, Pa CO2 is determined by the level of alveolar ventilation according to the following equation (a restatement of the equation given above for alveolar ventilation): Pa CO2 = VCO2 K/VA where K is a constant (0.863). The relation between Pa CO2 and alveolar ventilation is hyperbolic. As ventilation decreases below 4-6 L/min, Pa CO2 rises precipitously. A decrease in alveolar ventilation can result from a reduction in overall (minute) ventilation or an increase in the proportion of dead space ventilation. A reduction in minute ventilation is observed primarily in the setting of neuromuscular disorders and CNS depression. In pure hypercapnic respiratory failure, the hypoxemia is easily corrected with oxygen therapy. Hyperventilation is an uncommon cause of respiratory failure and usually occurs from depression of the CNS from drugs or neuromuscular diseases affecting respiratory muscles. Hypoventilation is characterized by hypercapnia and hypoxemia. Hypoventilation can be differentiated from other causes of hypoxemia by the presence of a normal alveolar-arterial PO2 gradient.

ETIOLOGY These diseases can be grouped according to the primary abnormality and the individual components of the respiratory system (eg, CNS, peripheral nervous system, respiratory muscles, chest wall, airways, and alveoli). A variety of pharmacologic, structural, and metabolic disorders of the CNS are characterized by depression of the neural drive to breathe. This may lead to acute or chronic hypoventilation and hypercapnia. Examples include tumors or vascular abnormalities involving the brain stem, an overdose of a narcotic or sedative, and metabolic disorders such as myxedema or chronic metabolic alkalosis.

Disorders of the peripheral nervous system, respiratory muscles, and chest wall lead to an inability to maintain a level of minute ventilation appropriate for the rate of carbon dioxide production. Concomitant hypoxemia and hypercapnia occur. Examples include Guillain-Barr syndrome, muscular dystrophy, myasthenia gravis, severe kyphoscoliosis, and morbid obesity. Severe airway obstruction is a common cause of acute and chronic hypercapnia. Examples of upper-airway disorders are acute epiglottitis and tumors involving the trachea; lower-airway disorders include COPD, asthma, and cystic fibrosis. Diseases of the alveoli are characterized by diffuse alveolar filling, frequently resulting in hypoxemic respiratory failure, although hypercapnia may complicate the clinical picture. Common examples are cardiogenic and noncardiogenic pulmonary edema, aspiration pneumonia, or extensive pulmonary hemorrhage. These disorders are associated with intrapulmonary shunt and an increased work of breathing. Common causes : Type I (hypoxemic) respiratory failure include the following: Type II (hypercapnic) respiratory failure include the following:

the thorax, such as abdominal pain or long-bone fracture. Neurologic manifestations include restlessness, anxiety, confusion, seizures, or coma. Asterixis may be observed with severe hypercapnia. Tachycardia and a variety of arrhythmias may result from hypoxemia and acidosis. Cyanosis, a bluish color of skin and mucous membranes, indicates hypoxemia. Visible cyanosis typically is present when the concentration of deoxygenated hemoglobin in the capillaries or tissues is at least 5 g/dL. Dyspnea, an uncomfortable sensation of breathing, often accompanies respiratory failure. Excessive respiratory effort, vagal receptors, and chemical stimuli (hypoxemia and/or hypercapnia) all may contribute to the sensation of dyspnea. Both confusion and somnolence may occur in respiratory failure. Myoclonus and seizures may occur with severe hypoxemia. Polycythemia is a complication of long-standing hypoxemia. Pulmonary hypertension frequently is present in chronic respiratory failure. Alveolar hypoxemia potentiated by hypercapnia causes pulmonary arteriolar constriction. If chronic, this is accompanied by hypertrophy and hyperplasia of the affected smooth muscles and narrowing of the pulmonary arterial bed. The increased pulmonary vascular resistance increases afterload of the right ventricle, which may induce right ventricular failure. This, in turn, causes enlargement of the liver and peripheral edema. The entire sequence is known as cor pulmonale. Criteria for the diagnosis of ARDS include the following:

COPD Pneumonia Pulmonary edema Pulmonary fibrosis Asthma Pneumothorax Pulmonary embolism Pulmonary arterial hypertension Pneumoconiosis Granulomatous lung diseases Cyanotic congenital heart disease Bronchiectasis Acute respiratory distress syndrome (ARDS) Fat embolism syndrome Kyphoscoliosis Obesity

COPD Severe asthma Drug overdose Poisonings Myasthenia gravis Polyneuropathy Poliomyelitis Primary muscle disorders Porphyria Cervical cordotomy Head and cervical cord injury Primary alveolar hypoventilation Obesity-hypoventilation syndrome Pulmonary edema ARDS Myxedema Tetanus

Clinical presentation - Tachypnea and dyspnea; crackles upon auscultation Clinical setting - Direct insult (aspiration) or systemic process causing lung injury (sepsis) Radiologic appearance - 3-quadrant or 4-quadrant alveolar flooding Lung mechanics - Diminished compliance (< 40 mL/cm H2 O) Gas exchange - Severe hypoxia refractory to oxygen therapy (ratio of arterial oxygen tension to fractional concentration of oxygen in inspired gas [PaO2/FI O2] < 200) Normal pulmonary vascular properties - Pulmonary capillary wedge pressure lower than 18 mm Hg Diagnostic Considerations Respiratory failure is a common and a life-threatening condition that demands prompt diagnosis and assessment and appropriate management. Failure to visualize an obvious abnormality on chest radiographs in hypoxemic respiratory failure suggests the possibility of right-to-left shunting. The vast majority of patients in acute respiratory failure due to cardiogenic pulmonary edema respond to measures to reduce preload and afterload. Those with acute respiratory distress syndrome (ARDS) require early elective intubation because the duration of respiratory failure is longer. Hypercapnic respiratory failure occurs secondary to a variety of causes, including an increased respiratory muscle load, impaired neuromuscular function, and decreased respiratory drive caused by central nervous system (CNS) depression.

PHYSICAL ASSESSMENT The signs and symptoms of acute respiratory failure reflect the underlying disease process and the associated hypoxemia or hypercapnia. Localized pulmonary findings reflecting the acute cause of hypoxemia (eg, pneumonia, pulmonary edema, asthma, or chronic obstructive pulmonary disease [COPD]), may be readily apparent. In patients with ARDS, the manifestations may be remote from

DIAGNOSTIC TEST

Pulmonary Function Tests Patients with acute respiratory failure generally are unable to perform PFTs; however, these tests are useful in the evaluation of chronic respiratory failure.

Respiratory failure may be associated with a variety of clinical manifestations. However, these are nonspecific, and very significant respiratory failure may be present without dramatic signs or symptoms. This emphasizes the importance of measuring arterial blood gases in all patients who are seriously ill or in whom respiratory failure is suspected. Chest radiography is essential. Echocardiography is not routinely done but is sometimes useful. Pulmonary functions tests (PFTs), if feasible, may be helpful. Electrocardiography (ECG) should be performed to evaluate the possibility of a cardiovascular cause of respiratory failure; it also may detect dysrhythmias resulting from severe hypoxemia or acidosis. Right-heart catheterization is controversial. LABORATORY STUDIES Once respiratory failure is suspected on clinical grounds, arterial blood gas analysis should be performed to confirm the diagnosis and to assist in the distinction between acute and chronic forms. This helps assess the severity of respiratory failure and helps guide management. A complete blood count (CBC) may indicate anemia, which can contribute to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory failure. A chemistry panel may be helpful in the evaluation and management of a patient in respiratory failure. Abnormalities in renal and hepatic function may either provide clues to the etiology of respiratory failure or alert the clinician to complications associated with respiratory failure. Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure and other organ function. Measuring serum creatine kinase with fractionation and troponin I helps exclude recent myocardial infarction in a patient with respiratory failure. An elevated creatine kinase level with a normal troponin I level may indicate myositis, which occasionally can cause respiratory failure. In chronic hypercapnic respiratory failure, serum levels of thyroid-stimulating hormone (TSH) should be measured to evaluate the possibility of hypothyroidism, a potentially reversible cause of respiratory failure. Echocardiography Echocardiography need not be performed routinely in all patients with respiratory failure. However, it is a useful test when a cardiac cause of acute respiratory failure is suspected. The findings of left ventricular dilatation, regional or global wall motion abnormalities, or severe mitral regurgitation support the diagnosis of cardiogenic pulmonary edema. A normal heart size and normal systolic and diastolic function in a patient with pulmonary edema would suggest ARDS. Echocardiography provides an estimate of right ventricular function and pulmonary artery pressure in patients with chronic hypercapnic respiratory failure.

Normal values for forced expiratory volume in 1 second (FEV 1) and forced vital capacity (FVC) suggest a disturbance in respiratory control. A decrease in the FEV 1 -to-FVC ratio (FEV1/FVC) indicates airflow obstruction, whereas a reduction in both FEV1 and FVC and maintenance of FEV1/FVC suggest restrictive lung disease. Respiratory failure is uncommon in obstructive diseases when FEV1 is greater than 1 L and in restrictive diseases when FVC is greater than 1 L.

RADIOGRAPHY Chest radiography is essential in the evaluation of respiratory failure because it frequently reveals the cause (see the images below). However, distinguishing between cardiogenic and noncardiogenic pulmonary edema is often difficult. Increased heart size, vascular redistribution, peribronchial cuffing, pleural effusions, septal lines, and perihilar bat-wing distribution of infiltrates suggest hydrostatic edema; the lack of these findings suggests acute respiratory distress syndrome (ARDS). TREATMENTS Approach Considerations The risks of oxygen therapy are oxygen toxicity and carbon dioxide narcosis. Pulmonary oxygen toxicity rarely occurs when a fractional concentration of oxygen in inspired gas (F I O2) lower than 0.6 is used; therefore, an attempt to lower the inspired oxygen concentration to this level should be made in critically ill patients. Carbon dioxide narcosis occasionally occurs when some patients with hypercapnia are given oxygen to breathe. Arterial carbon dioxide tension (P a CO2) increases sharply and progressively with severe respiratory acidosis, somnolence, and coma. The mechanism is primarily the reversal of pulmonary vasoconstriction and the increase in dead space ventilation. Hypoxemia is the major immediate threat to organ function. After the patients hypoxemia is corrected and the ventilatory and hemodynamic status have stabilized, every attempt should be made to identify and correct the underlying pathophysiologic process that led to respiratory failure in the first place. The specific treatment depends on the etiology of respiratory failure. Patients generally are prescribed bed rest during early phases of respiratory failure management. However, ambulation as soon as possible helps ventilate atelectatic areas of the lung. Consultation with a pulmonary specialist and an intensivist are often required. Patients with acute respiratory failure or exacerbations of chronic respiratory failure need to be admitted to the intensive care unit for ventilatory support.

CORRECTION OF HYPOXEMIA The first objective in the management of respiratory failure is to reverse and/or prevent tissue hypoxia. Hypercapnia unaccompanied by hypoxemia generally is well tolerated and probably is not a threat to organ function unless accompanied by severe acidosis. Many experts believe that hypercapnia should be tolerated until the arterial blood pH falls below 7.2. Appropriate management of the underlying disease obviously is an important component in the management of respiratory failure. A patient with acute respiratory failure generally should be admitted to a respiratory care unit or intensive care unit (ICU). Most patients with chronic respiratory failure can be treated at home with oxygen supplementation and/or ventilatory assist devices along with therapy for their underlying disease. Extracorporeal membrane oxygenation (ECMO) may be more effective than conventional management for patients with severe but potentially reversible respiratory failure. Peek et al found that survival without severe disability was significantly higher in patients who were [7] transferred to a single specialized center for consideration of ECMO. In a randomized, controlled trial in 180 patients either with a Murray lung injury score of 3.0 or higher or with uncompensated hypercapnia and a pH lower than 7.20 despite optimal conventional treatment, 36.7% of patients in the ECMO arm had died or were severely disabled 6 months after randomization, compared with 52.9% of patients in the conventional treatment arm. Although average total costs were more than twice as high for ECMO than for conventional care in this study, lifetime quality-adjusted life-years (QALYs) gained were 10.75 for the ECMO group and [7] 7.31 for the conventional group. Assurance of an adequate airway is vital in a patient with acute respiratory distress. The most common indication for endotracheal intubation is respiratory failure. Endotracheal intubation serves as an interface between the patient and the ventilator. Another indication is airway protection in patients with altered mental status. Once the airway is secured, attention is turned toward correcting the underlying hypoxemia, the most life-threatening facet of acute respiratory failure. The goal is to assure adequate oxygen delivery to tissues, generally achieved with an arterial oxygen tension (P a O2) of 60 mm Hg or an arterial oxygen saturation (Sa O2) greater than 90%. Supplemental oxygen is administered via nasal prongs or face mask; however, in patients with severe hypoxemia, intubation and mechanical ventilation are often required. Coexistent hypercapnia and respiratory acidosis may have to be addressed. This is done by correcting the underlying cause or providing ventilatory assistance. PRINCIPLES OF MECHANICAL VENTILATION Mechanical ventilation is used for 2 essential reasons: (1) to increase P a O2 and (2) to lower Pa CO2. Mechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue. The use of mechanical ventilation during the polio epidemics of the 1950s was the impetus that led to the development of the discipline of critical care medicine. Before the mid-1950s, negativepressure ventilation with the use of iron lungs was the predominant method of ventilatory support.

Currently, virtually all mechanical ventilatory support for acute respiratory failure is provided by positive-pressure ventilation. Nevertheless, negative-pressure ventilation still is used occasionally in patients with chronic respiratory failure.

Types of mechanical ventilation Over the years, mechanical ventilators have evolved from simple pressure-cycled machines to sophisticated microprocessor-controlled systems. The following is a brief overview of the basic principles of their use. Positive-pressure versus negative-pressure ventilation For air to enter the lungs, a pressure gradient must exist between the airway and the alveoli. This can be accomplished either by raising pressure at the airway (positive-pressure ventilation) or by lowering pressure at the level of the alveolus (negative-pressure ventilation). The iron lung or tank ventilator is the most common type of negative-pressure ventilator used in the past. These ventilators work by creating subatmospheric pressure around the chest, thereby lowering pleural and alveolar pressure and facilitating flow of air into the patients lungs. These ventilators are bulky and poorly tolerated and are not suitable for use in modern critical care units. Positive-pressure ventilation can be achieved via an endotracheal or tracheostomy tube or noninvasively through a nasal mask or face mask. Controlled versus patient-initiated ventilation Ventilatory assistance can be controlled or patient-initiated. In controlled ventilation, the ventilator delivers assistance independent of the patients own spontaneous inspiratory efforts. In contrast, during patient-initiated ventilation, the ventilator delivers assistance in response to the patients own inspiratory efforts. The patients inspiratory efforts can be sensed either by pressure or flowtriggering mechanisms. Pressure-targeted versus volume-targeted ventilation During positive-pressure ventilation, either pressure or volume may be set as the independent variable. In volume-targeted (or volume preset) ventilation, tidal volume is the independent variable set by the physician or respiratory therapist, and airway pressure is the dependent variable. In this type of ventilation, airway pressure is a function of the set tidal volume and inspiratory flow rate, the patients respiratory mechanics (compliance and resistance), and the patients respiratory muscle activity. In pressure-targeted (or pressure preset) ventilation, airway pressure is the independent variable, and tidal volume is the dependent variable. The tidal volume during pressure-targeted ventilation is a complex function of inspiratory time, the patients respiratory mechanics, and the patients own respiratory muscle activity.

Endotracheal intubation Mechanical ventilation requires an interface between the patient and the ventilator. In the past, this invariably occurred through an endotracheal or tracheostomy tube, but there is a growing trend toward noninvasive ventilation, which can be accomplished by the use of either a full face mask [8] (covering both the nose and mouth) or a nasal mask (see Noninvasive Ventilatory Support). Care of an endotracheal tube includes correct placement of the tube, maintenance of proper cuff pressure, and suctioning to maintain a patent airway. After intubation, the position of the tube in the airway (rather than the esophagus) should be confirmed by auscultation of the chest and, ideally, by a carbon dioxide detector. As a general rule, the endotracheal tube should be inserted to an average depth of 23 cm in men and 21 cm in women (measured at the incisor). Confirming proper placement of the endotracheal tube with a chest radiograph is recommended. The tube should be secured to prevent accidental extubation or migration into the mainstem bronchus, and the endotracheal tube cuff pressure should be monitored periodically. The pressure in the cuff generally should not exceed 25 mm Hg. Endotracheal suctioning can be accomplished via either open-circuit or closed-circuit suction catheters. Routine suctioning is not recommended, because suctioning may be associated with a variety of complications, including desaturation, arrhythmias, bronchospasm, severe coughing, and introduction of secretions into the lower respiratory tract. Ventilator modes Pressure support ventilation (PSV) can be categorized as patient-initiated, pressure-targeted ventilation. With PSV, ventilatory assistance occurs only in response to the patient s spontaneous inspiratory efforts. With each inspiratory effort, the ventilator raises airway pressure by a preset amount. When the inspiratory flow rate decays to a minimal level or to a percentage of initial inspiratory flow (eg, 25% of peak flow), inspiration is terminated. During PSV, patients are free to choose their own respiratory rate; inspiratory time, inspiratory flow rate, and tidal volume are determined, in part, by the patients respiratory efforts. This mode of ventilation should not be used in patients with unstable ventilatory drive, and care must be exercised when the patients respiratory mechanics are changing because of bronchospasm, secretions, or varying levels of autopositive end-expiratory pressure (auto-PEEP). Intermittent mandatory ventilation (IMV) is a mode whereby mandatory breaths are delivered at a set frequency, tidal volume, and inspiratory flow rate. However, the patient can breathe spontaneously between the machine-delivered breaths. Most modern ventilators are capable of synchronized IMV (SIMV), whereby the ventilator attempts to deliver the mandatory breaths in synchrony with the patients own inspiratory efforts. In essence, the ventilator allows the patient an opportunity to breathe. If the patient makes an inspiratory effort during a window of time determined by the IMV rate, the ventilator delivers a mandatory breath in response to the patients inspiratory effort. However, if no inspiratory effort is detected by the ventilator, a time-triggered breath is delivered. Compared with standard IMV, SIMV may improve patient comfort and may limit dynamic hyperinflation, which may occur when a preset breath is delivered immediately after the patients spontaneous inspiratory effort (ie, before exhalation).

In assist-control ventilation, patients receive a fixed tidal volume and inspiratory flow rate with each inspiratory effort, regardless of their respiratory rate. However, a backup rate is selected that guarantees that the patient receives a minimum number of breaths per minute. If the patients respiratory rate falls below the backup rate, the ventilator delivers the number of breaths necessary to reach that rate; such breaths are delivered independent of any inspiratory effort by the patient. In volume-control mode, respiratory rate, tidal volume, and inspiratory flow rate (or inspiratory time) are fixed. This mode is used most often in heavily sedated or paralyzed patients. In pressure-control mode, as contrasted with volume-control mode, airway pressure is raised by a set amount at a fixed number of times per minute. The physician or respiratory therapist also sets the inspiratory-to-expiratory (I:E) ratio or the inspiratory time. This mode is used most often in heavily sedated or paralyzed patients. Pressure-control inverse-ratio ventilation (PCIRV) is a variation of simple pressure-control ventilation. In this mode, inspiration is set to be longer than expiration. The I:E ratio should rarely, if ever, exceed 3:1. Triggering mechanisms In patient-initiated (assisted) ventilation, the ventilator must sense the patients inspiratory effort in order to deliver assistance. Ventilator triggering may be based on a change in either pressure or flow. With pressure triggering, the ventilator is set to detect a certain change in pressure. The ventilator is triggered whenever airway pressure drops by the set amount. For example, in a patient on no positive end-expiratory pressure (PEEP) with a trigger sensitivity set at 1 cm H2 O, a breath is triggered whenever airway pressure falls below 1 cm H2 O. In a patient on 5 cm H2 O PEEP with the same trigger sensitivity, a breath is triggered whenever airway pressure falls below +4 cm H 2 O. With flow triggering, a continuous flow of gas is sent through the ventilator circuit. In some ventilators, this continuous flow rate may be set by the physician or respiratory therapist, whereas in other ventilators, the continuous flow rate is fixed. A flow sensitivity is selected, and the ventilator senses the patients inspiratory efforts by detecting a change in flow. When the patient makes an inspiratory effort, some of the gas that was previously flowing continuously through the circuit is diverted to the patient. The ventilator senses the decrease in flow returning through the circuit, and a breath is triggered. One problem with flow triggering is that automatic triggering sometimes results from leaks in the ventilator circuit. Positive end-expiratory pressure By maintaining airway (and hence alveolar) pressure greater than zero, PEEP may recruit atelectatic alveoli and prevent their collapse during the succeeding expiration. PEEP also shifts lung water from the alveoli into the perivascular interstitial space and helps with recruitment of alveoli. However, it does not decrease the total amount of extravascular lung water. In patients with disorders such as acute respiratory distress syndrome (ARDS) or acute lung injury (ALI), PEEP is applied to recruit atelectatic alveoli, thereby improving oxygenation and allowing a reduction in FI O2 to nontoxic levels (< 0.6). Applying PEEP of 3-5 cm H2 O to prevent a decrease in functional residual capacity in patients with normal lungs is a common practice.

In an ARDS Network trial, higher PEEP produced better oxygenation and lung compliance but no [3] benefit to survival, time on ventilator, or nonpulmonary organ dysfunction. Although sufficient PEEP is essential in ventilator management of patients with ARDS, this level varies from patient to patient. Ideal PEEP helps to achieve adequate oxygenation and decrease the requirement for high fractions of inspiratory oxygen without causing any of the harmful effects of PEEP. Current evidence does not support routine application of high PEEP strategy in people with ALI or ARDS; however, a study by Briel et al found higher PEEP levels have been associated with [9] improved survival among patients with ARDS. PEEP causes an increase in intrathoracic pressure, which may decrease venous return and cardiac output, particularly in patients with hypovolemia. Inspiratory flow In volume-targeted ventilation, inspiratory flow is a variable that is set by the physician or respiratory therapist. The inspiratory flow rate is selected on the basis of a number of factors, including the patients inspiratory drive and the underlying disease. Two flow patterns are used commonly: (1) a constant-flow (ie, square-wave) pattern (see the image below) and (2) a decelerating-flow pattern. With a constant-flow pattern, inspiratory flow is held constant throughout the breath, whereas with a decelerating-flow pattern, flow rises quickly to a maximal value and then decreases progressively throughout the breath.

cause barotrauma. In critically ill patients, the manifestations of barotrauma can be subtle. For example, the earliest sign of pneumothorax in supine patients may be the deep-sulcus sign or a collection of air anteriorly along cardiophrenic angle. It is now recognized that lung damage indistinguishable from ARDS may be caused by certain patterns of ventilatory support. Early animal experiments showed that mechanical ventilation employing high peak airway pressures and high tidal volume led to pulmonary edema, possibly as a result of direct parenchymal injury and altered microvascular permeability secondary to high peak alveolar pressures. Subsequent work indicates that excessive tidal volumes resulting in alveolar overdistention are the most important factor in ventilator-associated lung injury. A strategy of using low tidal volumes in patients with ARDS who are on mechanical ventilation has led to a reduced incidence of barotrauma and improved survival rates in clinical trials. Weaning From Ventilator Weaning or liberation from mechanical ventilation is initiated when the underlying process that necessitated ventilatory support has improved. In some patients, such as those recovering from uncomplicated major surgery or a toxic ingestion, withdrawal of ventilator support may be done without weaning. In patients who required more prolonged respiratory therapy, the process of liberating the patient from ventilatory support may take much longer. A patient who has stable underlying respiratory status, adequate oxygenation (eg, Pa O2/ FI O2 >200 on PEEP < 10 cm H2 O), intact respiratory drive, and stable cardiovascular status should be considered for discontinuance of mechanical ventilation. Many criteria have been used to predict success in weaning, including a minute ventilation of less than 10 L/min, maximal inspiratory pressure more than 25 cm water, vital capacity more than 10 mL/kg, absence of dyspnea, absence of paradoxical respiratory muscle activity, and agitation or tachycardia during the weaning trial. However, the rapid-shallow breathing indexthat is, the patients tidal volume (in liters) divided by the respiratory rate (in breaths/min) during a period of spontaneous breathingmay be a better predictor of successful extubation. In one study, a daily trial of spontaneous breathing in patients with a rapid-shallow breathing index of less than 105 resulted in a shorter duration of mechanical ventilation. A spontaneous breathing trial of only 30 minutes appears adequate to identify patients in whom successful extubation is likely. In patients who are not yet ready to be liberated from the ventilator, one should focus on the cause of ventilator dependency, such as excessive secretions, inadequate respiratory drive, impaired cardiac function, and ventilatory muscle weakness, rather than the type of ventilator or the mode of assistance. The weaning protocol could be designed with assist-control ventilation, with gradually increasing time spent in trials of spontaneous breathing or by gradually reducing the level of PSV. SIMV appears to result in less rapid weaning than PSV or trials of spontaneous breathing. Patientventilator desynchrony is an important component in a carefully designed weaning protocol. Attention must be directed toward patient comfort, avoidance of fatigue, adequate nutrition, and prevention and treatment of medical complications during the weaning period. Peak inspiratory and plateau pressures should be assessed frequently. Attempts should be made to limit the plateau pressure to less than 25 cm H2 O. Expiratory volume is checked initially and

Wave forms of a volume-targeted ventilator: Pressure, flow, and volume waveforms are shown with square-wave flow pattern. A is baseline, B is increase in tidal volume, C is reduced lung compliance, and D is increase in flow rate. All 3 settings lead to increase in peak airway pressures. Adapted from Spearman CB et al. In pressure-targeted ventilation, the inspiratory flow rate is a dependent variable that varies as a function of the preset pressure and the patients own inspiratory effort. Because airway pressure is held constant while alveolar pressure rises during inspiration, the pressure difference between airway and alveoli decreases, leading to a decelerating pattern of inspiratory flow. Ventilator-associated lung injury Mechanical ventilation is associated with a variety of insults to the lung. In the past, physicians focused on barotrauma, including pneumothorax, pneumomediastinum, and subcutaneous and pulmonary interstitial emphysema. The manifestations of barotrauma probably result from excessive alveolar wall stress; excessive airway pressure by itself does not appear to

periodically (continuously if ventilator-capable) to assure that the set tidal volume is delivered. In patients with severe airflow obstruction, auto-PEEP (PEEPi) should be monitored on a regular basis.

taking medications regularly, weight loss, and avoiding medications and foods that can potentially elevate blood pressure should be emphasized. Staging of Hypertension

HYPERTENSIVE CARDIOVASCULAR DISEASE Overview The cause of hypertensive heart disease is chronically elevated blood pressure (BP); however, the causes of elevated BP are diverse. Essential hypertension accounts for 90% of cases of hypertension in adults. Secondary causes ofhypertension account for the remaining 10% of cases of chronically elevated BP. According to the Framingham Study, hypertension accounts for about one quarter of heart [1] failure cases. In the elderly population, as many as 68% of heart failure cases are attributed to [2] hypertension. Community-based studies have demonstrated that hypertension may contribute to the development of heart failure in as many as 50-60% of patients. In patients with hypertension, the risk of heart failure is increased by 2-fold in men and by 3-fold in women. Cardiovascular effects of hypertension Uncontrolled and prolonged elevation of BP can lead to a variety of changes in the myocardial structure, coronary vasculature, and conduction system of the heart. These changes in turn can lead to the development of left ventricular hypertrophy (LVH), coronary artery disease (CAD), various conduction system diseases, and systolic and diastolic dysfunction of the myocardium, complications that manifest clinically as angina or myocardial infarction, cardiac arrhythmias (especially atrial fibrillation), and congestive heart failure (CHF). Thus, hypertensive heart disease is a term applied generally to heart diseases, such as LVH (seen in the images below), coronary artery disease, cardiac arrhythmias, and CHF, that are caused by the direct or indirect effects of elevated BP. Although these diseases generally develop in response to chronically elevated BP, marked and acute elevation of BP can lead to accentuation of an underlying predisposition to any of the symptoms traditionally associated with chronic hypertension.

Although hypertensive heart disease typically is not described in various stages, the disease usually progresses in the following sequence:

Increased wall stress leads to LVH Which leads to diastolic LV dysfunction Which can be followed by systolic LV dysfunction The risks of ventricular ectopy, ventricular arrhythmias, sudden cardiac death, and cardiovascular mortality are increased in patients once LVH develops and are also increased in patients with heart failure. Table 1, below, shows the division of BP and hypertension into stages. Table 1. Stages of Elevated BP and Hypertension According to The Seventh Report of the Joint National Committee (JNC7) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure Systolic BP, mm Hg Diastolic BP, mm Hg < 80 80-89 90-99 >100

Category

Optimal

< 120

Prehypertension 120-139 Stage I Stage II 140-159 >160

Laboratory Studies Differentials The following conditions should also be considered when evaluating hypertensive heart disease: Laboratory studies are helpful in establishing the etiology of hypertension, quantitating the severity of target organ damage, and monitoring the adverse effects of therapy. The tests to be ordered depend on clinical judgment regarding the etiology of hypertension. Recommendations from the Seventh Report of the Joint National Committee (JNC7) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure include carrying out the following baseline laboratory workup before initiating treatment for hypertension :

Coronary artery atherosclerosis 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 Sleep apnea Patient education It is important to educate patients about the nature of their disease and the risks associated with untreated hypertension. In addition, dietary modifications and the importance of regular exercise,

Electrocardiogram Urinalysis Blood glucose and hematocrit levels Serum potassium, creatinine (or the corresponding estimated glomerular filtration rate [GFR]), and calcium measurements Lipid profile after a 9- to 12-hour fast - Includes high density lipoprotein (HDL) cholesterol, lowdensity lipoprotein (LDL) cholesterol, and triglycerides

Optional tests - Include measurement of urinary albumin excretion or albumin/creatinine ratio Evaluating the renal system Blood urea nitrogen (BUN) and creatinine levels are elevated in patients with renal failure. Other studies include the above-mentioned urinalysis, GFR, and urinary albumin excretion or albumin/creatinine ratio measurements. Evaluating the endocrine system Hypokalemia is found in patients with primary hyperaldosteronism and in patients with secondary hyperaldosteronism, Cushing disease, and Bartter syndrome. Hypokalemia is most useful in leading to further diagnostic studies if the patient has not received diuretics. Plasma renin activity is generally depressed and serum aldosterone level is elevated in patients with primary hyperaldosteronism. Twenty-four hour urinary catecholamine and metanephrine levels are elevated in patients with pheochromocytoma. Elevated 24-hour urinary free cortisol and failure to suppress an early morning serum cortisol level after an overnight dexamethasone suppression test are observed in patients with Cushing disease. Thyrotropin levels may be elevated in patients with hypothyroidism and depressed in patients with hyperthyroidism.

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