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In addition to the mechanism described above, a number of other medical conditions may cause syncope. Making the correct diagnosis for loss of consciousness is difficult. The core of the diagnosis of vasovagal syncope rests upon a clear description of a typical pattern of triggers, symptoms, and time course.
It is pertinent to differentiate lightheadedness, seizures, vertigo, and low blood sugar as other causes.
In people with recurrent vasovagal syncope, diagnostic accuracy can often be improved with one of the following diagnostic tests:
- A tilt table test (results should be interpreted in the context of patients' clinical presentations and with an understanding of the sensitivity and specificity of the test)
- Implantation of an insertable loop recorder
- A Holter monitor or event monitor
- An echocardiogram
- An electrophysiology study
Treatment for reflex syncope focuses on avoidance of triggers, restoring blood flow to the brain during an impending episode, and measures that interrupt or prevent the pathophysiologic mechanism described above.
People with POTS will show a marked rise in heart rate within 10 minutes of standing or being tilted 60° head-up on a tilt table, without a corresponding decrease in blood pressure. A variety of autonomic tests are employed to exclude autonomic disorders that could underlie symptoms, while endocrine testing is used to exclude hyperthyroidism and rarer endocrine conditions. Electrocardiography is normally performed on all patients to exclude other possible causes of tachycardia. In cases where a particular associated condition or complicating factor are suspected, other non-autonomic tests may be used: echocardiography to exclude mitral valve prolapse, and thermal threshold tests for small-fiber neuropathy.
Testing the cardiovascular response to prolonged head-up tilting, exercise, eating, and heat stress may help determine the best strategy for managing symptoms. POTS has also been divided into several types (see § Causes), which may benefit from distinct treatments. People with neuropathic POTS show a loss of sweating in the feet during sweat tests, as well as impaired norepinephrine release in the leg, but not arm. This is believed to reflect peripheral sympathetic denervation in the lower limbs. People with hyperadrenergic POTS show a marked increase of blood pressure and norepinephrine levels when standing, and are more likely to suffer from prominent palpitations, anxiety, and tachycardia.
POTS has a favorable prognosis when managed appropriately. Symptoms improve within five years of diagnosis for many patients, and 60% return to their original level of functioning. About 90% of people with POTS respond to a combination of pharmacological and physical treatments. Those who develop POTS in their early to mid teens during a period of rapid growth will most likely see complete symptom resolution in two to five years. Outcomes are more guarded for adults newly diagnosed with POTS. Some people do not recover, and a few even worsen with time. The hyperadrenergic type of POTS typically requires continuous therapy. If POTS is caused by another condition, outcomes depend on the prognosis of the underlying disorder.
The diagnosis of hypotension is made by first obtaining a blood pressure, either non-invasively with a sphygmomanometer or invasively with an arterial catheter (mostly in an intensive care setting). If the MAP (Mean Arterial Pressure) is <65mmHg, this is generally considered hypotension.
For most adults, the healthiest blood pressure is at or below 120/80 mmHg. A small drop in blood pressure, even as little as 20 mmHg, can result in transient hypotension.
Evaluation of vasovagal syncope is done with a tilt table test.
Hypotension is low blood pressure, especially in the arteries of the systemic circulation. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood. A systolic blood pressure of less than 90 millimeters of mercury (mm Hg) or diastolic of less than 60 mm Hg is generally considered to be hypotension. However, in practice, blood pressure is considered too low only if noticeable symptoms are present.
Hypotension is the opposite of hypertension, which is high blood pressure. It is best understood as a physiological state, rather than a disease. Severely low blood pressure can deprive the brain and other vital organs of oxygen and nutrients, leading to a life-threatening condition called shock.
For some people who exercise and are in top physical condition, low blood pressure is a sign of good health and fitness.
For many people, excessively low blood pressure can cause dizziness and fainting or indicate serious heart, endocrine or neurological disorders.
Treatment of hypotension may include the use of intravenous fluids or vasopressors. When using vasopressors, trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve a MAP of greater than 65 mm Hg in adults.
According to current guidelines, requirements for diagnosis with sepsis are "the presence (probable or documented) of infection together with systemic manifestations of infection". These manifestations may include:
- Tachypnea (fast rate of breathing), which is defined as more than 20 breaths per minute, or when testing blood gas, a less than 32 mmHg, which signifies hyperventilation
- White blood cell count either significantly low ( 12000 cells/mm)
- Tachycardia (rapid heart rate), which in sepsis is defined as a rate greater than 90 beats per minute
- Altered body temperature: Fever > or hypothermia <
Documented evidence of infection, may include positive blood culture, signs of pneumonia on chest x-ray, or other radiologic or laboratory evidence of infection. Signs of end-organ dysfunction are present in septic shock, including kidney failure, liver dysfunction, changes in mental status, or elevated serum lactate.
Septic shock is diagnosed if there is low blood pressure (BP) that does not respond to treatment. This means that intravenous fluid administration alone is not enough to maintain a patient's BP. Diagnosis of septic shock is made when systolic blood pressure is less than 90mm Hg, a mean arterial pressure (MAP) is less than 70 mm Hg, or a systolic BP decreases 40 mm Hg or more without other causes for low BP.
Postpartum chills is a physiological response that occurs within two hours of childbirth. It appears as uncontrollable shivering that is not under voluntary control. It is seen in many women after delivery and can be unpleasant. It lasts for a short time. It is thought to be a result of a nervous system response. It may also be related to fluid shifts and the actual strenuous work of labor. It is considered a normal response and there is no accompanying fever. If a fever does develop further assessments may reveal the presence of an infection. Treatment consists of an explanation from clinicians that the shivering is a normal response and that it only lasts for a short time. Warm blankets are given to the women and fluid replacement is encouraged. It has been described as a fairly common and normal occurrence.
After discharge to home with the baby, chills that accompany uncontrolled bleeding, shortness of breath, cold clammy skin, dizziness, heart pain, and racing heart can be a sign of shock that needs immediate medical attention. Mastitis can also cause shivering.
The medical literature suggests a number of treatments that have been proven effective for specific cases of needle phobia, but provides very little guidance to predict which treatment may be effective for any specific case. The following are some of the treatments that have been shown to be effective in some specific cases.
- Ethyl Chloride Spray (and other freezing agents). Easily administered, but provides only superficial pain control.
- Jet Injectors. Jet Injectors work by introducing substances into the body through a jet of high pressure gas as opposed to by a needle. Though these eliminate the needle, some people report that they cause more pain. Also, they are only helpful in a very limited number of situations involving needles i.e. insulin and some inoculations.
- Iontophoresis. Iontophoresis drives anesthetic through the skin by using an electric current. It provides effective anesthesia, but is generally unavailable to consumers on the commercial market and some regard it as inconvenient to use.
- EMLA. EMLA is a topical anesthetic cream that is a eutectic mixture of lidocaine and prilocaine. It is a prescription cream in the United States, and is available without prescription in some other countries. Although not as effective as iontophoresis, since EMLA does not penetrate as deeply as iontophoresis-driven anesthetics, EMLA provides a simpler application than iontophoresis. EMLA penetrates much more deeply than ordinary topical anesthetics, and it works adequately for many individuals.
- Ametop. Ametop gel appears to be more effective than EMLA for eliminating pain during venepuncture.
- Lidocaine/tetracaine patch. A self-heating patch containing a eutectic mixture of lidocaine and tetracaine is available in several countries, and has been specifically approved by government agencies for use in needle procedures. The patch is sold under the trade name "Synera" in the United States and "Rapydan" in European Union. Each patch is packaged in an air-tight pouch. It begins to heat up slightly when the patch is removed from the packaging and exposed to the air. The patch requires 20 to 30 minutes to achieve full anesthetic effect. The Synera patch was approved by the United States Food and Drug Administration on 23 June 2005.
- Behavioral therapy. Effectiveness of this varies greatly depending on the person and the severity of the condition. There is some debate as to the effectiveness of behavioral treatments for specific phobias (like blood, injection, injury type phobias), though some data are available to support the efficacy of approaches like exposure therapy. Any therapy that endorses relaxation methods may be contraindicated for the treatment of fear of needles as this approach encourages a drop in blood pressure that only enhances the vasovagal reflex. In response to this, graded exposure approaches can include a coping component relying on applied tension as a way to prevent complications associated with the vasovagal response to specific blood, injury, injection type stimulus.
- Nitrous Oxide (Laughing Gas). This will provide sedation and reduce anxiety for the patient, along with some mild analgesic effects.
- Inhalation General Anesthesia. This will eliminate all pain and also all memory of any needle procedure. On the other hand, it is often regarded as a very extreme solution. It is not covered by insurance in most cases, and most physicians will not order it. It can be risky and expensive and may require a hospital stay.
- Benzodiazepines, such as diazepam (Valium) or lorazepam, may help alleviate the anxiety of needle phobics, according to Dr. James Hamilton. These medications have an onset of action within 5 to 15 minutes from ingestion. A relatively large oral dose may be necessary.
Exercise hypertension is an excessive rise in blood pressure during exercise. Many of those with exercise hypertension have spikes in systolic pressure to 250 mmHg or greater.
A rise in systolic blood pressure to over 200 mmHg when exercising at 100 W is pathological and a rise in pressure over 220 mmHg needs to be controlled by the appropriate drugs.
Similarly, in healthy individuals the response of the diastolic pressure to 'dynamic' exercise (e.g. walking, running or jogging) of moderate intensity is to remain constant or to fall slightly (due to the improved blood flow), but in some individuals a rise of 10 mmHg or greater is found.
Recent work at Johns Hopkins involving a group of athletes aged 55 to 75 with mild hypertension has found a correlation of those with exercise hypertension to a reduced ability of the major blood vessels to change in size in response to increased blood flow (probably due to impaired function of the endothelial cells in the vessel walls). This is to be differentiated from stiffness of the blood-vessel walls, which was not found to be correlated with the effect.
Fear of needles, especially in its more severe forms, is often comorbid with other phobias and psychological ailments; for example, iatrophobia, or an irrational fear of doctors, is often seen in needle phobic patients.
A needle phobic patient does not need to physically be in a doctor's office to experience panic attacks or anxiety brought on by needle phobia. There are many triggers in the outside world that can bring on an attack through association. Some of these are blood, injuries, the sight of the needle physically or on a screen, paper pins, examination rooms, hospitals, white lab coats, hospital gowns, doctors, dentists, nurses, the antiseptic smell associated with offices and hospitals, the sight of a person who physically resembles the patient's regular health care provider, or even reading about the fear.
Because lowered blood pressure in septic shock contributes to poor perfusion, fluid resuscitation is an initial treatment to increase blood volume. Crystalloids such as normal saline and lactated Ringer's solution are recommended as the initial fluid of choice, while the use of colloid solutions such as hydroxyethyl starch have not shown any advantage or decrease in mortality. When large quantities of fluids are given, administering albumin has shown some benefit.
ADT tachyphylaxis specifically occurs in depressed patients using SSRIs and MAOIs. Currently, SSRIs are the preferred treatment for depression among clinicians, as MAOIs require the patient to avoid certain foods and other medications due to the potential for interactions capable of inducing dangerous side effects. Provided is a list of medications known to be subject to Poop-out.
The first line of defense in preventing chronic Somogyi rebound is additional blood glucose testing. Continuous blood glucose monitoring is the preferred method to detect and prevent the Somogyi rebound, but this technology is not yet widely used. Alternatively, testing blood sugar more often, 8 to 10 times daily with a traditional blood glucose meter, facilitates detecting the low blood sugar level before such a rebound occurs.
Testing occasionally during the middle of the night is also important, particularly when high waking blood sugars are found, to determine if more insulin is needed to prevent hyperglycemia or if less insulin is needed to prevent such a rebound.
Sometimes a person with diabetes will experience the Somogyi rebound when awake and notice symptoms of the initial low blood sugar or symptoms of the rebound. At night, waking with a night sweat (perhaps combined with a rapid heart rate) is a symptom of the adrenaline and rebound. Unfortunately, the evidence shows that patients with type 1 diabetes do not normally wake during nocturnal hypoglycemic episodes.
While reviewing log data of blood glucose after the fact, signs of Somogyi rebound should be suspected when blood glucose numbers seem "higher" after the insulin dosage has been raised, particularly in the morning. One simple way to determine if nocturnal hypoglycemia may be causing morning hyperglycemia is to have the patient have a high protein snack with a small amount of carbohydrates at bedtime. This will help keep the blood sugar up overnight and prevent the somogyi effect. If the morning blood sugar decreases, this is indicative of the somogyi effect and the daily insulin should be decreased.
In theory, avoidance is simply a matter of preventing hyperinsulinemia. In practice, the difficulty for a diabetic person to aggressively dose insulin to keep blood sugars levels close to normal and at the same time constantly adjust the insulin regimen to the dynamic demands of exercise, stress, and wellness can practically assure occasional hyperinsulinemia. The pharmacokinetic imperfections of all insulin replacement regimens is a severe limitation.
Some practical behaviors which are useful in avoiding chronic Somogyi rebound are:
- frequent blood glucose monitoring (8–10 times daily);
- continuous blood glucose monitoring;
- logging and review of blood glucose values, searching for patterns of low blood sugar values;
- conservative increases in insulin delivery;
- awareness to the signs of hypoglycemia;
- awareness to hyperglycemia in response to increased delivery of insulin;
- use of appropriate types of insulin (long-acting, short-acting, etc.) in appropriate amounts.
Hypertrophy of the ventricle can be measured with a number of techniques.
Electrocardiogram (EKG), a non-invasive assessment of the electrical system of the heart, can be useful in determining the degree of hypertrophy, as well as subsequent dysfunction it may precipitate. Specifically, increase in Q wave size, abnormalities in the P wave as well as giant inverted T waves are indicative of significant concentric hypertrophy. Specific changes in repolarization and depolarization events are indicative of different underlying causes of hypertrophy and can assist in appropriate management of the condition. Changes are common in both eccentric and concentric hypertrophy, though are substantially different from one another. In either condition fewer than 10% of patients with significant hypertrophy display a normal EKG.
Transthoracic echocardiography, a similarly non invasive assessment of cardiac morphology, is also important in determining both the degree of hypertrophy, underlying pathologies (such as aortic coarction), and degree of cardiac dysfunction. Important considerations in echocardiography of the hypertrophied heart include lateral and septal wall thickness, degree of outflow tract obstruction, and systolic anterior wall motion (SAM) of the mitral valve, which can exacerbate outflow obstruction.
It is not uncommon to undergo cardiopulmonary exercise testing (CPET), which measures the heart's response to exercise, to assess the functional impairment caused by hypertrophy and to prognosticate outcomes.
Patients affected by ADT tachyphylaxis experience a noticeably sudden progressive decrease in response to SSRIs. The reported rates of this condition vary from 9% to 33% of SSRI users, and the majority of those affected are less responsive to subsequent treatments. In most observational studies, these individuals suffer a recurrence or relapse of depression without changing the previously effective dose.
ADT tachyphylaxis incorporates drug sensitivity as a potential causal factor for the decreased response. However, tolerance provides a more accurate explanation. While the exact cause of ADT tachyphylaxis in individual cases is unknown, drug tolerance is a more comprehensive model, as it includes mechanisms of pharmacodynamic tolerance, metabolic tolerance, and others.
Patients are typically sent to therapy for BII phobia in order to receive therapeutic treatments to calm their levels of anxiety and stress. Therapists use a combination of psychological and physical measures, such as applying muscle tension, in order to help the patient to be aware that there is certainly a needle in front of them.
A popular method of treatment for BII phobics is Cognitive-Behavior Therapy (CBT), which is a technique that allows the patient to become immune to their fear by being exposed to it. For BII phobics, patients are given pictures of needles or blood, they are also asked to draw pictures of these needles and speak about it. Afterwards, they are given an actual needle, and the goal is: by that point, that the patient is to be comfortable enough with their fear of needles and blood.
Some patients may refuse professional help for their phobia. Instead, a different type of treatment solely revolves around motivation and whether or not the patient is willing to undergo through treating their phobia with self-help. Similar to CBT, patients treat themselves by completing exercises to become immune to their fear. This requires no professional assistance and merely relies on the person.
Research on hypnotherapy has been looked upon to treat patients with BII phobia. Hypnotherapists are known for using relaxing therapies towards individuals with common anxiety issues. A form of therapy given to patients with BII phobia include the “Applied Tension” method, which was developed by Lars-Göran Öst and his colleagues at the University of Uppsala in Sweden. This “coping method involves creating tension on a person’s arms, legs, and chest until they start to feel their body temperature rising,” (Robertson) which usually occurs within 10 to 20 seconds. These sessions of muscle tension is repeated 5 times with 20 to 30 second breaks. Patients should complete this form of therapy over the course of 5 weeks. This helps to prevent the patient from fainting by applying tension to the body, the blood pressure steadily rises, preventing any sudden drop until their vaccination is complete. By using this treatment, there was a noticeable improvement by 90% of patients with BII phobia. Compared to patients that only used the relaxation methods, where only 60% showed noticeable improvement.
Along with muscle tension,there are several methods of physical maneuvers that can help with the treatment of BII phobia. Therapists suggest that while being injected, patients should perform movements, such as: leg crossing, muscle tensing, and holding in the breath. Patients are instructed by their therapist to perform these maneuvers simultaneously while being injected with a needle. It’s also recommended that the patient stays seated with their head lowered while performing these movements.
Acute stress reaction (also called acute stress disorder, psychological shock, mental shock, or simply shock) is a psychological condition arising in response to a terrifying or traumatic event, or witnessing a traumatic event that induces a strong emotional response within the individual. It should not be confused with the unrelated circulatory condition of shock/hypoperfusion. Acute stress reaction (ASR) may develop into delayed stress reaction (better known as PTSD) if stress is not correctly managed. ASR is characterized by re-living and avoiding reminders of an aversive event, as well as generalized hypervigilance after initial exposure to a traumatic event. ASD is differentiated from PTSD as a disorder that precedes it, and if symptoms last for more than one month, it will develop into PTSD. It can thus be thought of as the acute phase of PTSD.
In most situations, described above, the increase in ventricular wall thickness is a slow process. However, in some instances hypertrophy may be "dramatic and rapid." In the Burmese python, consumption of a large meal is associated with an increase in metabolic work by a factor of seven and a 40% increase in ventricular mass within 48 hours, both of which return to normal within 28 days.
Psychedelics such as LSD-25 and psilocybin-containing mushrooms demonstrate very rapid tachyphylaxis. In other words, one may be unable to 'trip' two days in a row. Some people are able to 'trip' by taking up to three times the dosage, yet some users may not be able to negate tachyphylaxis at all until a period of days has gone by.
To discover the extent and severity of coronary artery ectasia there are a variety of diagnostic tools used. The most common method for discovering the disease is through angiography. Angiography is the procedure where a contrast dye is entered into the vessels and an x-ray is taken, which will allow the vessels to be seen on the x-ray. Using angiography clinicians are able to display the size, location and number of vessels affected by the disease. Is can also be analyzed through other methods such as intravascular ultrasound, and magnetic resonance imaging. Using these diagnostic methods, it has been discovered that the disease normally occurs most often in the right coronary artery, followed by the left anterior descending artery, and finally the left anterior circumflex artery. Using these methods Coronary artery ectasia can be divided into four different types: Type 1¬→diffuse ectasia in 2-3 different vessels, Type 2¬→ diffuse disease in 1 vessel and local disease in another, Type 3¬→ diffuse disease in one vessel and Type 4¬→ localized or segmental ectasia.
In a patient fully withdrawn from opioids, going back to an intermittent schedule or maintenance dosing protocol, a fraction of the old tolerance level will rapidly develop, usually starting two days after therapy is resumed and, in general, leveling off after day 7. Whether this is caused directly by opioid receptors modified in the past or affecting a change in some metabolic set-point is unclear. Increasing the dose will usually restore efficacy; relatively rapid opioid rotation may also be of use if the increase in tolerance continues.
This disorder may resolve itself with time or may develop into a more severe disorder such as PTSD. However, results of Creamer, O'Donnell, and Pattison's (2004) study of 363 patients suggests that a diagnosis of acute stress disorder had only limited predictive validity for PTSD. Creamer et al. did find that re-experiences of the traumatic event and arousal were better predictors of PTSD. Early pharmacotherapy may prevent the development of posttraumtic symptoms.
Studies have been conducted to assess the efficacy of counselling and psychotherapy for people with ASD. Cognitive behavioral therapy which included exposure and cognitive restructuring was found to be effective in preventing PTSD in patients diagnosed with ASD with clinically significant results at 6 months follow-up. A combination of relaxation, cognitive restructuring, imaginal exposure, and in vivo exposure was superior to supportive counseling. Mindfulness based stress reduction programs also appear to be effective for stress management.
In a wilderness context where counseling, psychotherapy, and cognitive behavioral therapy is unlikely to be available, the treatment for acute stress reaction is very similar for the treatment of cardiogenic shock, vascular shock, and hypovolemic shock; that is, allowing the patient to lie down, providing reassurance, and removing the stimulus for the occurrence of the reaction. In traditional shock cases, this is generally the relieving of pain from injuries or the stopping of blood loss. In an acute stress reaction, this may be pulling a rescuer away from the emergency to calm down, or blocking the sight of an injured friend from a patient.
BII phobia is one of the more common psychiatric disorders, affecting about 3 to 4% of the general population, and in about 80% of the BII phobia cases, the patient experiences syncope or presyncope. After a random survey was completed in Aligarh, India, with 1648 male and 1613 female, it was found that a significantly higher percentage of females compared to males had BII phobia; 23.36% of females were diagnosed with BII phobia while only 11.19% of males were diagnosed. Females also fainted more often than males, at 64.09% compared to a male rate of 39.4%.
Furthermore, only 5.3% of BII phobia patients reported to have visited the hospital once or twice for consultation about BII phobia, however, without engaging in any kind of treatment.
Another study, involving participants from all 50 states and the District of Columbia, ages 65 years and older, found that a total of 386 participants disclosed having BII Phobia throughout their whole lifetime, 90% of those cases consisted of patients dealing with BII Phobia as well as other lifetime fears.