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The uses, pharmacology, clinical efficacy, dosage and administration, adverse effects, and drug interactions of hawthorn are discussed. Hawthorn (Crataegus oxyacantha) is a fruit-bearing shrub with a long history as a medicinal substance. Uses have included the treatment of digestive ailments, dyspnea, kidney stones, and cardiovascular disorders. Today, hawthorn is used primarily for various cardiovascular conditions. The cardiovascular effects are believed to be the result of positive inotropic activity, ability to increase the integrity of the blood vessel wall and improve coronary blood flow, and positive effects on oxygen utilization. Flavonoids are postulated to account for these effects. Hawthorn has shown promise in the treatment of New York Heart Association (NYHA) functional class II congestive heart failure (CHF) in both uncontrolled and controlled clinical trials. There are also suggestions of a beneficial effect on blood lipids. Trials to establish an antiarrhythmic effect in humans have not been conducted. The recommended daily dose of hawthorn is 160-900 mg of a native water-ethanol extract of the leaves or flowers (equivalent to 30-169 mg of epicatechin or 3.5-19.8 mg of flavonoids) administered in two or three doses. At therapeutic dosages, hawthorn may cause a mild rash, headache, sweating, dizziness, palpitations, sleepiness, agitation, and gastrointestinal symptoms. Hawthorn may interact with vasodilating medications and may potentiate or inhibit the actions of drugs used for heart failure, hypertension, angina, and arrhythmias. The limited data about hawthorn suggest that it may be useful in the treatment of NYHA functional class II CHF.
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PMID:Hawthorn: pharmacology and therapeutic uses. 1188 7

Cardiac arrhythmias are a well known cause of mortality for patients with heart disease. However, sinus tachycardia is a more unusual arrhythmia which can lead to serious heart damage or death. Even young patients with structurally normal hearts may become gravely ill. This case study outlines the condition of sinus tachycardia, and associated changes in heart function, altered cellular structure of the myocardium and compensatory mechanisms in the body. Treatment modalities, including electro-physiological studies and drug therapies to moderate the tachycardia and myocardial oxygen demand of the heart, are discussed. Fourteen year old 'Ben' was previously a well, active and outgoing youth who suddenly became critically ill. He endured weeks of hospitalisation, numerous serious complications including Torsade de pointes arrhythmia, Cheyne-Stokes respirations, nausea and dizziness during this acute phase. Despite challenges, Ben's severely compromised heart muscle recovered at a remarkable rate.
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PMID:Tachycardia's toll: tachycardia induced cardiomyopathy--a case study. 1259 74

Carbon monoxide (CO) is a colorless, tasteless, odorless, and non-irritating gas formed when carbon in fuel is not burned completely. It enters the bloodstream through the lungs and attaches to hemoglobin (Hb), the body's oxygen carrier, forming carboxyhemoglobin (COHb) and thereby reducing oxygen (O(2)) delivery to the body's organs and tissues. High COHb concentrations are poisonous. Central nervous system (CNS) effects in individuals suffering acute CO poisoning cover a wide range, depending on severity of exposure: headache, dizziness, weakness, nausea, vomiting, disorientation, confusion, collapse, and coma. At lower concentrations, CNS effects include reduction in visual perception, manual dexterity, learning, driving performance, and attention level. Earlier work is frequently cited to justify the statement that CO exposure sufficient to produce COHb levels of ca. 5% would be sufficient to produce visual sensitivity reduction and various neurobehavioral performance deficits. In a recent literature re-evaluation, however, the best estimate was that [COHb] would have to rise to 15-20% before a 10% reduction in any behavioral or visual measurement could be observed. This conclusion was based on (1) critical review of the literature on behavioral and sensory effects, (2) review and interpretation of the physiological effects of COHb on the CNS, (3) extrapolation from the effects of hypoxic hypoxia to the effects of CO hypoxia, and (4) extrapolation from rat behavioral effects of CO to humans. Also covered in this review article are effects of chronic CO exposure, the discovery of neuroglobin, a summary of the relatively new role for endogenous CO in neurotransmission and vascular homeostasis, groups which might be especially sensitive to CO, and recommendations on further research. The interested reader is directed to other published reviews of the literature on CO and historically seminal references that form our understanding of this ubiquitous gas.
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PMID:Carbon monoxide and the nervous system. 1266 97

The 'Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - International Consensus on Science' recommend an artificial ventilation volume of 10 ml/kg bodyweight (equivalent to a tidal volume of 700-1000 ml) without the use of supplemental oxygen in adults with respiratory arrest. For first aid providers using the mouth-to-mouth or mouth-to-nose-ventilation technique, respectively, a ventilation volume of approximately 9.6 l/min results. Additionally, a deep breath is recommended before each ventilation to increase the end-expiratory oxygen concentration of the air exhaled by the first aid provider. To investigate the effects of these recommendations in healthy volunteers, test persons were asked to ventilate an artificial lung model for a period of up to 10 min. The tidal volume was set at 800 ml at a breathing rate of 12/min. End-tidal carbon dioxide, oxygen saturation (measured by pulse oximetry), and heart rate were measured continuously. Capillary blood gas samples were collected and non-invasive blood pressure readings were recorded prior to the start of ventilation and immediately after the end of the measuring period. The data reveal a statistically significant and clinically relevant decrease in end-tidal carbon dioxide pressure (P<0.001, median decrease 14 mmHg), and the occurrence of hyperventilation-associated symptoms such as paraesthesia, dizziness, and carpopedal spasms in more than 75% of the participants. Clinically and statistically significant hyperventilation results in first aid providers performing artificial ventilation according to the guidelines. This artificial ventilation is associated with a significant decrease in capillary and end-tidal carbon dioxide pressure as well as with multiple symptoms of an acute hyperventilation syndrome. Ventilation performed according to these guidelines may cause injury to the health of the first aid provider. Rescuers ventilating the victim should be replaced at regular intervals and the recommendation to take a deep breath before each ventilation should not be upheld in order to minimise the risk of hyperventilation.
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PMID:Artificial ventilation for basic life support leads to hyperventilation in first aid providers. 1280 4

Most cases of ARF are secondary to volume depletion. In the literature, very few scientific publications address the problem of what to do when confronted with such a patient. As regarding the diagnosis of hypovolemia, an accurate history and physical examination can help to determine both the presence and etiology of volume depletion; postural hypotension (decrement in systolic blood pressure of more than 20 mmHg after standing from the supine position), associated with a pulse increment of 30 beats/min or more and dizziness are specific symptoms of hypovolemia. Laboratory indices are useful to diagnose volume depletion, but their interpretation is not simple, and they may not be available in the non-nephrologic environment. Fluid replacement therapy in hypovolemia is largely dependent upon the type of fluid that has been lost and concurrent electrolytic and acid-base disorders. Patients with hypernatremia and volume depletion should receive mild hypotonic solutions, whereas those with hyponatremia and hypovolemia should receive mild hypertonic solutions. The entity of reinfusion depends on daily losses. Conversely, monitoring of body weight can be considered an adequate index of fluid balance. Concerning the treatment of ARF, the use of loop diuretics in the early phases of pre-renal ARF decrease oxygen consumption in the tubular cells by inhibiting transcellular sodium transport, therefore preventing or limiting ischemic cell injury. The use of loop diuretics should also be evaluated in intermediate syndrome and ischemic NTA where diuretics can, respectively, reduce renal ischemia and convert oliguric ARF into the non-oliguric form.
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PMID:[Clinical management of the patient affected with acute renal failure (ARF) secondary to volume depletion]. 1452 97

Anemia, "tired blood," with all the accompanying symptoms, such as fatigue, dyspnea, dizziness, muscle weakness, altered brain function, decreased gastrointestinal function, and cardiac stress, is not a disease. Rather, anemia is a sign that something has interfered with the red blood cell transport system that carries hemoglobin-containing oxygen to all bodily tissues (National Anemia Action Council [NAAC], 2002). In part 1 of this discussion (May/June issue of Orthopaedic Nursing), anemias related to interference with red blood cell development were addressed. In this section, anemias related to hemoglobin abnormalities (microcytic hypochromic anemia) and anemias related to premature erythrocyte destruction (hemolytic anemia) are discussed. Treatment approaches and selected pharmacological interventions are identified.
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PMID:Tired blood. Part 2. 1459 97

The purpose of this study was to investigate the association between low blood pressure (BP) with mild symptoms of orthostatism, sleep-disordered breathing (SDB) and tilt test results in 7- to 12-y-old children. A retrospective chart review of 301 children, ages 7 to 12 y, was initially performed to evaluate the frequency of abnormal BP measurements. Then a prospective study was performed on 7- to 12-y-old prepubertal children with SDB, looking for both abnormal BP and mild orthostatism. All children had polysomnography. Those identified with abnormal (high or low) BP measurements (called "BP outliers") were studied with a new polysomnogram followed by a head-up tilt test as an indicator of autonomic activity. Four of the children with low BP were treated with nasal continuous positive airway pressure and received a second head-up tilt test 3.5 to 7 mo after starting treatment. The prospective study included 78 children, eight of whom were BP outliers. Seven of these outliers had low BP. Compared with all of the SDB subjects, SDB subjects with low BP and indicators of mild orthostatic hypotension had a significantly higher incidence of craniofacial dysmorphism, symptoms of SDB early in life, chronically cold extremities, and dizziness on standing up (chi2, p = 0.01 to 0.0001). They had a significantly greater drop in BP without evidence of autonomic neuropathy than all other children on head-up tilt testing (Kruskal-Wallis ANOVA with Bonferroni adjustment, p = 0.001 to 0.0001). However, the normotensive SDB controls also had significantly different BP drops than the normal controls (p = 0.0001). The four children placed on nasal continuous positive airway pressure had a nonsignificant trend toward normalization of tilt test response. SDB in prepubertal children can lead to different abnormal stimulation of the autonomic nervous system, with different impacts on BP. The severity and frequency of oxygen saturation drops during sleep, nonhypoxic increases in respiratory effort, and the duration of abnormal breathing are suspected of playing a role in the difference in autonomic nervous system stimulation.
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PMID:Abnormal blood pressure in prepubertal children with sleep-disordered breathing. 1460 62

Bosentan is a nonpeptide, specific, competitive, dual antagonist at both endothelin receptor subtypes (ET(A) and ET(B)). Orally administered bosentan effectively prevents endothelin 1-induced vasoconstriction in pulmonary vessels in patients with pulmonary arterial hypertension. Improvement in exercise capacity from baseline was significantly greater with bosentan than with placebo in two phase III trials in patients with WHO functional class III or IV pulmonary arterial hypertension (primary or associated with connective tissue disease) despite treatment with vasodilators, diuretics, anticoagulants, cardiac glycosides, or supplemental oxygen. The beneficial effects of bosentan on exercise capacity were maintained for at least 20 weeks. Compared with placebo, bosentan led to a significantly greater improvement from pretreatment values in secondary efficacy endpoints such as the Borg dyspnea index, WHO functional class, and cardiopulmonary hemodynamic parameters (cardiac index, pulmonary vascular resistance, pulmonary artery pressure, pulmonary capillary wedge pressure, mean right atrial pressure). Bosentan significantly reduced the incidence, and delayed the onset, of clinical worsening of pulmonary arterial hypertension compared with placebo. In published clinical trials, adverse events that occurred with similar or greater frequency with bosentan 125 mg twice daily than with placebo included headache, syncope, flushing and abnormal hepatic function. Those that occurred less frequently with bosentan 125 mg twice daily than with placebo included dizziness, worsening of symptoms of pulmonary arterial hypertension, cough and dyspnea.
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PMID:Bosentan. 1472 63

A 27-year-old flight instructor experienced 5 to 10 minutes after a scuba-dive to 29 m, which lasted totally 50 minutes, dizziness, nausea and severe vertigo. The symptoms lasted about an hour. The patient vomited several times and noted sudden onset headache and vertigo lasting the following three days. Hyperbaric oxygen therapy was started 30 hours after the event because decompression sickness was suspected. Transthoracic echocardiographic evaluation showed a patent foramen ovale. Diving accidents may be caused by decompression sickness, the formation of a free intravascular gas phase (bubbles) may result in transatrial shunting in the presence of a patent foramen ovale and may lead to neurological signs and symptoms. In this context the diver was advised to undergo closure of the atrial septal defect. Five months after the incident the patient underwent successful transcatheter occlusion of the PFO.
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PMID:[Severe vertigo after a scuba-dive to 29 meters]. 1517 13

PRESENTING FEATURES: A 53-year-old man who had human immunodeficiency virus (HIV) presented to the Johns Hopkins Hospital with a 3-month history of increasing dysphagia, cough, dyspnea, chest pain, and an episode of syncope. His past medical history was notable for oral and presumptive esophageal candidiasis that was treated with fluconazole 6 months prior to presentation. Three months prior to presentation, he discontinued his medications, and his symptoms of dysphagia recurred. During that time he developed intermittent fevers and chills, progressively worsening dyspnea on exertion, and a cough productive of white sputum. He also reported a 40-lb weight loss over the past 3 months. On the day prior to presentation, he had chest pain and shortness of breath followed by weakness, dizziness, and a brief syncopal episode. He denied orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, jaundice, hemoptysis, hematemesis, melena, hematochezia, or diarrhea. There was no history of alcohol use, and he stopped smoking tobacco approximately 1 month previously. He smoked cocaine but denied injection drug use. The patient had never been on antiretroviral therapy and had never had his CD4 count or viral load measured. On physical examination, the patient was a thin, cachectic man who appeared older than his stated age. His vital signs were notable for blood pressure of 102/69 mm Hg, resting tachycardia of 102 beats per minute, resting oxygen saturation of 92% on room air, normal resting respiratory rate, and a temperature of 38.1 degrees C. His oropharynx was clear, with no signs of thrush or mucosal ulcers. His pulmonary examination was notable for diminished breath sounds in the lower lung fields bilaterally. Cardiac, abdominal, and neurologic examinations were normal. His skin was intact, with no visible petechiae, rashes, nodules, or ulcers. Laboratory studies showed a total white blood cell count of 3.2 x 10(3)/microL, with a total lymphocyte count of 330/microL, hematocrit of 30.2%, a serum sodium level of 129 mEq/L, and a serum lactate dehydrogenase level of 219 IU/L. The patient had an absolute CD4 count of 8 cells/mm3 and a HIV viral load of 86,457 copies/mL. His arterial blood gas on room air had a pH of 7.51, a PCO2 of 33 mm Hg, and a PO2 of 55 mm Hg. Electrocardiogram and serial serum cardiac enzymes were normal. A chest radiograph showed bilateral upper lobe patchy infiltrates with left upper lobe consolidation. Computed tomographic (CT) scan of the chest with contrast showed bilateral ground glass infiltrates with focal consolidation (Figure 1) and no evidence of pulmonary embolism. Induced sputum was negative for Pneumocystis carinii, fungi, or acid-fast bacilli. A bronchoalveolar lavage was performed. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. Diagnosis: P. carinii pneumonia and primary pulmonary sporotrichosis. 1533 85


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