DEFINITION Acute respiratory failure (ARF) exists when the patient's breathing apparatus fails in its ability to maintain

arterial blood gases within the normal range. By definition, ARF is present when the blood gases demonstrate: An arterial oxygen tension (PaO2) of < 8 kPa (60 mmHg) with normal or low PaCO2 (Type I or hypoxaemic respiratory failure) Or An arterial carbon dioxide tension (PaCO2) of > 6.7 kPa usually accompanied by a fall in pH (<7.3,H+ > 45 n mols l-1) in addition to hypoxaemia (Type II or ventilatory respiratory failure) Hypoxaemia on its own does not always mean respiratory failure, for example, if the subject is at altitude or has a right to left shunt due to congenital heart disease. We are concerned only with ARF, one of the most dramatic and life threatening emergencies that the casualty officer and the house office may have to deal with in the hospital setting.

PATHOPHYSIOLOGY Any part of the respiratory system may be involved in the causation of a respiratory emergency, i.e.

The respiratory centre in the CNS The respiratory apparatus (e.g. chest wall and lungs) The respiratory muscles including the diaphragm, the main respiratory pump

The gas exchanging units in the lung i.e. the respiratory bronchioles and the alveoli It is pertinent to remember that in assessing patients with ARF, most attention is paid to what is happening at the alveolar level i.e. the blood gases Site Respiratory centre (CNS) Examples Depressant drugs, opiates; traumatic and ischaemic lesions Loss of respiratory sensitivity to CO2 Spinal injury, Guillain Barre, poliomyelitis Myasthenia, neuromuscular blocking drugs Myopathies, respiratory muscle fatigue in COPD Flail chest, pneumothorax, haemothorax Deformities, trauma (e.g. rib fractures), loss of optimal shape due to chronic lung hyperinflation Extrathoracic: foreign bodies, croup Intrathoracic: asthma, bronchiolitis, bronchitis Emphysema, pulmonary oedema, ARDS, pneumonia Pulmonary embolus, ARDS

SIGNS AND SYMPTOMS Generally, the patient becoming anxious and completely preoccupied with the necessity to concentrate every effort on ventilation heralds the onset of ARF. The eyes are closed, the accessory muscles of ventilation are fully used; often a characteristic position is adopted, such as sitting forward with drooling secretions, as in the child with acute epiglottitis. Hypoxia and hypercarbia produce characteristic effects on the CNS and cardiovascular system (CVS), for example: 1 Hypoxia: CNS - Uncooperative, confused, drunken-like state CVS - Bradycardia, variable blood pressure, cyanosis 2 Hypercarbia: CNS - Tremor and overt flap CVS - Raised pulse rate, peripheral vasodilation with pink peripheries, blood pressure changes are variable

Spinal cord and peripheral nerves Neuromuscular junction Muscle Pleura and thoracic cage

Airways

Gaseous exchange Lung vasculature

TREATMENT Whatever the cause, four important principles of treatment apply: (a) Establish an airway This applies particularly to the unconscious patient, e.g. due to overdose, general anaesthesia, CNS trauma and so on. The patient is placed on the side with the head down, and lower jaw pulled forward to prevent the tongue falling back and obstructing the upper airway. At this stage it may become obvious that the obstruction is due primarily to foreign bodies or vomit, so this must be cleared, if possible. Indications for artificial airways (1) Oropharyngeal: this is useful where it is expected that the patient will soon recover consciousness, e.g. post-operatively, or where there is lack of expertise in endotracheal intubation. A laryngeal mask may be used as an alternative in this situation (2) Endotracheal tube (ETt): If unconsciousness is expected to last for more than a matter of minutes, as in drug overdose, then an ETT must be used both to ensure and to protect the airway (e.g. from aspiration of gastric contents). If ventilation is depressed or inadequate due to trauma or disease, than mechanical ventilation will be required. (3) Cricothyrotomy and tracheostomy obstruction above the cords due to disease or infection may make intubation impossible. Cricothyrotomy or tracheostomy is then necessary to restore the airway. (4) Bronchoscopy may also be required for bronchial toilet, removing viscid mucous and obtaining specimens for microscopy and culture (b) Administer oxygen to ensure adequate tissue oxygenation (see this link) It is of paramount importance to maintain a PaO2 sufficient to give an arterial Hb saturation of at least 85% (i.e. 8-9 kPa or 60-70 mmHg). Hyperoxia should be avoided, particularly in the bronchitic who is a CO2 retainer and dependent on hypoxic ventilatory drive. (c) Maintain alveolar ventilation and treat underlying cause These two are inextricably linked. The causes of ARF are many and varied as are the requisite therapies. If treatment of the underlying cause is not successful (i.e. steroids, bronchodilators in asthma; physiotherapy, antibiotics, mucolytics, bronchodilators in acute or chronic bronchitis), then the carbon dioxide tension will begin to rise, necessitating intermittent positive pressure ventilation (IPPV). There is little place for respiratory stimulants, except perhaps narcotic antagonists in opiate overdose. NB Infection is a cause of exacerbation of ARF in bronchitics in less than 50% of cases. Other causes such as heart failure, dysrthymias and pneumothorax must be excluded and treated where necessary. In ARF due to chronic obstructive pulmonary disease (COPD), muscle fatigue is a major contributory factor to continuing hypoxia and hypercarbia. Non-invasive methods of ventilation (e.g. nasal mask) as well as endotracheal

intubation and IPPV may be needed. Pneumonia is an infection of the lung parenchyma. Community-acquired pneumonia refers to pneumonia acquired outside of hospitals or extended-care facilities. Nursing homeacquired pneumonia refers to infection acquired in an extended-care facility. Nosocomial pneumonia and hospital-acquired pneumonia describe infections acquired in the hospital setting. The signs and symptoms of acute pneumonia develop over hours to days, whereas the clinical presentation of chronic pneumonia often evolves over weeks to months. Streptococcus pneumoniae remains the most commonly identified pathogen in communityacquired pneumonia (Fig. 1). Other pathogens have been reported to cause pneumonia in the community, and their order of importance depends on the location and population studied (Table 1). These include long-recognized pathogens such asHaemophilus influenzae, Mycoplasma pneumoniae, and influenza A, along with newer pathogens such as Legionella species and Chlamydophilia pneumoniae. Other common causes in the immunocompetent patient include Moraxella catarrhalis, Mycobacterium tuberculosis, and aspiration pneumonia. The causative agent of community-acquired pneumonia remains unidentified in 30% to 50% of cases.5 Mechanism Inhalation of infectious particles Aspiration of oropharyngeal or gastric contents Hematogenous deposition Invasion from infection in contiguous structures Direct inoculation Reactivation Frequency Common Diagnostic: Radiography A cornerstone of diagnosis is the chest x-ray, which is recommended for diagnosis in every circumstance and usually reveals an infiltrate (Fig. 2) at presentation. Focal; large pleural effusion usually bacteria Cavitary - bacterial abscess, fungi, acid-fast bacilli, Nocardia Miliary acid-fast bacilli, fungi Rapod progression/multifocal Legionella spp., Pneumonococcus, Staphylococcus Insterstitial viruses, Pnumocystis jiroveci, Mycoplasma, Chlamydia psittaci Mediastinal widening without infiltrate Inhalation anthrax

Common

Uncommon

Rare

Less common More common in immunocompromised hosts

The aspiration of oropharyngeal or gastric contents is the most prevalent pathogenetic mechanism in nosocomial pneumonia, with several contributing factors. Swallowing and epiglottic closure may be impaired by neuromuscular disease, stroke, states of altered consciousness, or seizures. Endotracheal and nasogastric tubes interfere with these anatomic defenses and provide a direct route of entry for pathogens. Impaired lower esophageal sphincter function and nasogastric and gastrostomy tubes increase the risk of aspiration of gastric contents. Fortunately, aspiration rarely leads to overt bacterial pneumonia. Direct inoculation rarely occurs as a result of surgery or bronchoscopy but may play a role in the development of pneumonia in patients supported with mechanical ventilation. Hematogenous deposition of bacteria in the lungs is also uncommon but is responsible for some cases of pneumonia caused by S. aureus, Pseudomonas aeruginosa, andEscherichia coli. The direct extension of infection to the lung from contiguous areas, such as the pleural or subdiaphragmatic spaces, is rare. Reactivation of pathogens can take place in the setting of deficits of cell-mediated immunity. Pathogens such asPneumocystis jiroveci, Mycobacterium tuberculosis, and cytomegalovirus can remain latent for many years after exposure, with flares of active disease occurring in the presence of immune compromise. Reactivation tuberculosis occasionally occurs in immunocompetent hosts. Once bacteria reach the tracheobronchial tree, defects in local pulmonary defenses can make infection more likely. The cough reflex can be impaired by stroke, neuromuscular disease, sedatives, or poor nutrition. Mucociliary transport is depressed with the aging process, tobacco smoking, dehydration, morphine, atropine, prior infection with influenza virus, and chronic bronchitis. Anatomic changes such as

emphysema, bronchiectasis, and obstructive mass lesions prevent the clearance of microbes. Inflammatory cells drawn to infected areas of the pulmonary tree release proteolytic enzymes, altering the bronchial epithelium and ciliary clearance mechanisms and stimulating the production of excess mucus. Community-acquired MRSA strains contain Panton-Valentine leukocidin, a toxin that creates holes in neutrophil cell membranes, releasing chemotactic and inflammatory factors.7 A blunted cellular and humoral immune response can also increase the risk of pneumonia. For example, granulocyte chemotaxis is reduced with aging, diabetes mellitus, malnutrition, hypothermia, hypophosphatemia, and corticosteroids. Granulocytopenia may be caused by cytotoxic chemotherapy. Alveolar macrophages are rendered dysfunctional by corticosteroids, cytokines, viral illnesses, and malnutrition. Diminished antibody production or function can accompany hematologic malignancies such as multiple myeloma or chronic lymphocytic leukemia. Coronary heart disease (CHD) is a narrowing of the small blood vessels that supply blood and oxygen to the heart. CHD is also called coronary artery disease. Hardening of the arteries, also called atherosclerosis, is a common disorder. It occurs when fat, cholesterol, and other substances build up in the walls of arteries and form hard structures called plaques. Over time, these plaques can block the arteries and cause symptoms and problems throughout the body. Coronary heart disease (CHD) is the leading cause of death in the United States for men and women. Coronary heart disease is caused by the buildup of plaque in the arteries to your heart. This may also be called hardening of the arteries. Symptoms may be very noticeable, but sometimes you can have the disease and not have any symptoms. Chest pain or discomfort (angina) is the most common symptom. You feel this pain when the heart is not getting enough blood or oxygen. How bad the pain is varies from person to person. You may be asked to take one or more medicines to treat blood pressure, diabetes, or high cholesterol levels. Follow your doctor's directions closely to help prevent coronary artery disease from getting worse. Goals for treating these conditions in people who have coronary artery disease:

Fatty material and other substances form a plaque build-up on the walls of your coronary arteries. The coronary arteries bring blood and oxygen to your heart. This buildup causes the arteries to get narrow. As a result, blood flow to the heart can slow down or stop. A risk factor for heart disease is something that increases your chance of getting it. You cannot change some risk factors for heart disease, but others you can change. The risk factors for heart disease that you CANNOT change are:

It may feel heavy or like someone is squeezing your heart. You feel it under your breast bone (sternum), but also in your neck, arms, stomach, or upper back. The pain usually occurs with activity or emotion, and goes away with rest or a medicine called nitroglycerin. Other symptoms include shortness of breath and fatigue with activity (exertion). Women, elderly people, and people with diabetes are more likely to have symptoms other than chest pain, such as:

Blood pressure less than or equal to 140/90 (even lower for some patients with diabetes, kidney disease, or heart failure) Glycosylated hemoglobin (HbA1c) levels less than or equal to 7% for people with diabetes LDL cholesterol level less than or equal to 100 mg/dL (even lower for some patients) Treatment depends on your symptoms and how severe the disease is. Your doctor may give you one or more medicines to treat CHD, including:

Fatigue Shortness of breath Weakness

Your age. The risk of heart disease increases with age. Your gender. Men have a higher risk of getting heart disease than women who are still getting their menstrual period. After menopause, the risk for women is closer to the risk for men. See: Heart disease and women

ACE inhibitors to lower blood pressure and protect your heart and kidneys Aspirin, with or without clopidogrel (Plavix) or prasugrel (Effient) to help prevent blood clots from forming in your arteries Beta-blockers to lower heart rate, blood pressure, and oxygen use by the heart Calcium channel blockers to relax arteries, lower blood pressure, and reduce strain on the heart Diuretics ("water pills") to lower blood pressure and treat heart failure Nitrates (such as nitroglycerin) to stop chest pain and improve blood flow to the heart

Your genes. If your parents or other close relatives had heart disease, you are at higher risk. Your race. African Americans, Mexican Americans, American Indians, Hawaiians, and some Asian Americans also have a higher risk for heart problems.

Many things increase your risk for heart disease:

Statins to lower cholesterol

Diabetes is a strong risk factor for heart disease. High blood pressure increases your risks of heart disease and heart failure. Extra cholesterol in your blood builds up inside the walls of your heart's arteries (blood vessels). Smokers have a much higher risk of heart disease. Chronic kidney disease can increase your risk. People with narrowed arteries in another part of the body (examples are stroke and poor blood flow to the legs) are more likely to have heart disease. Substance abuse (such as cocaine) Being overweight

NEVER ABRUPTLY STOP TAKING ANY OF THESE DRUGS. Always talk to your doctor first. Stopping these drugs suddenly can make your angina worse or cause a heart attack. Your doctor may refer you to a cardiac rehabilitation program to help improve your heart's fitness. Procedures and surgeries used to treat CHD include:

Angioplasty and stent placement, called percutaneous coronary interventions (PCIs) Coronary artery bypass surgery Minimally invasive heart surgery

Not getting enough exercise, and feeling depressed or having excess stress are other risk factors Over the course of years and decades, plaque buildup narrows your arteries and makes them stiffer. These changes make it harder for blood to flow through them. Clots may form in these narrowed arteries and block blood flow. Pieces of plaque can also break off and move to smaller blood vessels, blocking them. Either way, the blockage starves tissues of blood and oxygen, which can result in damage or tissue death (necrosis).This is a common cause of heart attack and stroke. If a clot moves into an artery in the lungs, it can cause a pulmonary embolism. In some cases, the plaque is part of a process that causes a weakening of the wall of an artery. This can lead to an aneurysm. Aneurysms can break open (rupture), and cause bleeding that can be life threatening. Hardening of the arteries is a process that often occurs with aging. However, high blood cholesterol levels can make this process happen at a younger age. For most people, high cholesterol levels are the result of an unhealthy lifestyle -- most commonly, eating a diet that is high in fat. Other lifestyle factors are heavy alcohol use, lack of exercise, and being overweight. Other risk factors for hardening of the arteries are:

LIVE A HEALTHY LIFESTYLE Some of the risks for heart disease that you CAN change are:

Do not smoke or use tobacco.

Get plenty of exercise, at least 30 minutes a day on at least 5 days a week (talk to your doctor first). Maintain a healthy weight. Men and women should aim for a body mass index (BMI) between 18.5 and 24.9. Get checked and treated for depression. Women who are at high risk for heart disease should take omega-3 fatty acid supplements. If you drink alcohol, limit yourself to no more than one drink per day for women, and no more than two drinks per day for men.

Diabetes Family history of hardening of the arteries High blood pressure Smoking

Cerebral infarction is focal brain necrosis due to complete and prolonged ischemia that affects all tissue elements, neurons, glia, and vessels. Ischemic infarcts cause focal neurological deficits. In embolic infarcts, these appear abruptly. In atherothrombotic infarcts, they evolve over a period of time, usually hours. Atherothombotic infarcts are often preceded by transient ischemic attacks (TIAs). A TIA is a focal neurological deficit that lasts less than 24 hours and resolves. The mechanism of TIAs is uncertain. They may be caused by critical reduction of perfusion that impairs neurological function but falls short of causing permanent tissue damage, or by emboli that break up soon after they occlude vessels. The release of osmotically active substances (arachidonic acid, electrolytes, lactic acid) from the necrotic brain tissue causes cerebral edema. This is aggravated by vascular injury and leakage of proteins in the interstitial space. By 3-4 days, interstitial fluid accumulates in the infarct and around it. This is the most dangerous period for a large cerebral infarct. Death from a massive hemispheric infarct is caused by cerebral edema and herniations, not by the loss of brain tissue. Recovery of function, after an infarct, is due initially to restoration of perfusion in the penumbra (see below) and then to settling down of cerebral edema. Additional improvement may occur later through mechanisms involving neuronal plasticity.

CAUSES OF ISCHEMIC INFARCTION The diverse types of vascular disease and other conditions that cause cerebral infarction are partially listed in the table below and briefly discussed further on. Clinical classification systems for ischemic stroke, such as the TOAST (Trial of Org 10170 in Acute Stroke Treatment) and the ASCO (Atherosclerosis, Small vessel disease, Cardiac source, Other cause) systems have been introduced. These systems are based on clinical and ancillary findings, including noninvasive angiography and transthoracic echocardiography. Atherothrombosis, small vessel disease, and cardioembolism are the most common causes of ischemic stroke in elderly patients. Cardioembolism and the other entities listed can cause stroke in younger individuals, and some of them even in children. In the first day or so, the infarct appears as a poorly demarcated area of softening. CTImaging at this stage may be negative, especially in brain stem infarcts. MRI is much more sensitive. At the peak of edema, the infarct appears hypodense and bright on T2 MRI images. The infarcted tissue becomes sharply demarcated and softens progressively. From the second week onward, it begins todisintegrate and is gradually replaced by a cavity. The size and location of infarcts follows the anatomy of vascular territories. A large proportion of infarcts are caused by atherosclerosis of large arteries, alone or with superimposed thrombosis.

Causes of hyponatremia Many possible conditions and lifestyle factors can lead to hyponatremia, including:

Certain medications. Some medications, such as some antidepressants and pain medications, can cause you to urinate or perspire more than normal. Water pills (diuretics) especially thiazide diuretics. Diuretics work by making your body get rid of more sodium in urine. Cirrhosis. Liver disease can cause fluids to accumulate in your body. Kidney problems. Kidney failure and other kidney disease may make it hard to efficiently remove extra fluids from your body. Congestive heart failure. This condition causes your body to retain fluids. Syndrome of inappropriate anti-diuretic hormone (SIADH). In this condition, high levels of the anti-diuretic hormone (ADH) are produced, causing your body to retain water instead of excreting it normally in your urine. Drinking too much water during exercise (exertional hyponatremia). Because you lose sodium through sweat, drinking too much water during endurance activities, such as marathons and triathlons, can dilute the sodium content of your blood. Hormonal changes due to adrenal gland insufficiency (Addison's disease). Your adrenal glands produce hormones that help maintain your body's balance of sodium, potassium and water. Hormonal changes due to an underactive thyroid (hypothyroidism). Hypothyroidism may result in a low blood-sodium level. Primary polydipsia. In this condition, your thirst increases significantly, causing you to drink too much fluid. The recreational drug Ecstasy. This amphetamine increases the risk of severe and even fatal cases of hyponatremia. Chronic, severe vomiting or diarrhea. This causes your body to lose fluids and electrolytes, such as sodium. Dehydration. In dehydration, your body loses fluids and electrolytes. Diet. A low-sodium, high-water diet can sometimes disturb the proper balance between sodium and fluids in your blood.

The most common cause of genuinely high potassium (hyperkalemia) is related to your kidneys, such as: Chronic kidney failure Other causes of hyperkalemia include:

Acute kidney failure

Addison's disease (adrenal failure) Alcoholism or heavy drug use that causes rhabdomyolysis, a breakdown of muscle fibers that results in the release of potassium into the bloodstream Angiotensin-converting enzyme (ACE) inhibitors Destruction of red blood cells due to severe injury or burns Excessive use of potassium supplements Type 1 diabetes

Serum glutamic-pyruvic transaminase Serum glutamic-oxaloacetic transaminase Increased creatinine levels in the blood suggest diseases or conditions that affect kidney function. These can include:

Reduced blood flow to the kidney due to shock, dehydration, congestive heart failure, atherosclerosis, or complications of diabetes Creatinine blood levels can also increase temporarily as a result of muscle injury and are generally slightly lower duringpregnancy. Low blood levels of creatinine are not common, but they are also not usually a cause for concern. They can be seen with conditions that result in decreased muscle mass. Levels of 24-hour urine creatinine are evaluated with blood levels as part of a creatinine clearance test. Random urine creatinine levels have no standard reference ranges. They are usually used with other tests to reference levels of other substances measured in the urine. Some examples include the microalbumin test and urine protein test. POTENTIAL NURSING DIAGNOSIS FOR CHRONIC HEART FAILURE (CHF) 1. Decreased Cardiac output 2. Activity intolerance 3. Excess fluid volume 4. Risk for impaired gas exchange 5. Risk for impaired skin integrity

Damage to or swelling of blood vessels in the kidneys (glomerulonephritis) caused by, for example, infection orautoimmune diseases Bacterial infection of the kidneys (pyelonephritis) Death of cells in the kidneys small tubes (acute tubular necrosis) caused, for example, by drugs or toxins Prostate disease, kidney stone, or other causes of urinary tract obstruction

6. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs POTENTIAL NURSING DIAGNOSIS FOR ANGINA (CORONARY ARTERY DISEASE) 1. Acute pain 2. Risk for decreased cardiac output 3. Anxiety 4. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs POTENTIAL NURSING DIAGNOSIS FOR MYOCARDIAL INFARCTION 1. Acute pain 2. Activity intolerance 3. Anxiety/ Fear 4. Risk for decreased cardiac output 5. Ineffective tissue perfusion 6. Risk for excess fluid volume 7. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs POTENTIAL NURSING DIAGNOSIS FOR DYSRHYTHMIAS (INCLUDING DIGITALIS TOXICITY) 1. Risk for decreased cardiac output 2. Risk for poisoning, digitalis toxicity 3. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs POTENTIAL NURSING DIAGNOSIS FOR CARDIAC SURGERY: POSTOPERATIVE CARE CORONARY ARTERY BYPASS GRAFT (CABG), MINIMALLY INVASIVE DIRECT CORONARY ARTERY BYPASS (MIDCAB), CARDIOMYOPLASTY, VALVE REPLACEMENT 1. Risk for decreased cardiac output 2. Acute pain 3. Ineffective role performance 4. Risk for ineffective breathing pattern 5. Impaired skin integrity 6. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs

POTENTIAL NURSING DIAGNOSIS FOR THROMBOPHLEBITIS: DEEP VEIN THROMBOSIS (INCLUDING PULONARY EMBOLI CONSIDERATIONS) 1. Ineffective tissue perfusion 2. Acute pain 3. Impaired gas exchange (in presence of pulmonary embolus) 4. Deficient knowledge (Learning Need) regarding condition, treatment plan, self-care, and discharge needs The National Institutes of Health Stroke Scale (or NIHSS) is a method developed by the National Institutes of Health. It is used to gauge the severity of a stroke. [edit]NIH Stroke Scale

11. Extinction and Inattention: tests patient's recognition of self. Graded from 0-2. Scores range from 0-42. Patients are given more points for greater deficiencies. A score of "0" indicates that the test is normal.

1a. Level of Consciousness (LOC): tests stimulation. Graded from 0-3. 1b. LOC Questions: tests the patient's ability to answer questions correctly. Graded from 0-2. 1c. LOC Commands: tests the patient's ability to perform tasks correctly. Graded from 0-2. 2. Best Gaze: tests horizontal eye movements. Graded from 0-2. 3. Visual: tests visual fields. Graded from 0-3. 4. Facial Palsy: tests the patient's ability to move facial muscles. Graded from 0-3. 5. Motor Arm: tests motor abilities of the arms. Graded from 0-4. 6. Motor Leg: tests motor abilities of the legs. Graded from 0-4. 7. Limb Ataxia: tests coordination of muscle movements. Graded from 0-2. 8. Sensory: tests sensation of the face, arms, and legs. Graded from 0-2. 9. Best Language: tests the patient's comprehension and communication. Graded from 0-3. 10. Dysarthria: tests the patient's speech. Graded from 0-2.