How to Stop Heart Palpitations

Palpitations No More

Here are some of things included in the eBook, which you can download right now as a Pdf: Why no one else has offered you an effective solution so far. What the 3 most common reasons and treatment options are, and why they dont work. The 5 most common root causes of palpitations and how you can correct each one. How physical, mental, emotional problems can cause palpitations and how these can be prevented and corrected. How your diet can cause palpitations and how you can correct this to get results in as little as 24 hours. How a single little misalignment in your body can cause palpitations and other havoc, and how you can get this corrected. Learn how and why panic attacks develop and how you can use a simple technique to prevent them from occurring. and many other general health solutions.

Palpitations No More Overview


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Effects of Alcohol on the Cardiovascular System

Alcohol affects both the heart and the peripheral vasculature. Acutely, alcohol causes peripheral vasodilatation, giving a false sensation of warmth that can be dangerous. Heat loss is rapid in cold weather or when swimming, but reduced awareness leaves people vulnerable to hypothermia. The main adverse effect of acute alcohol on the cardiovascular system is the induction of arrhythmias. These are often harmless and experienced as palpitations but can rarely be fatal. Chronic ethanol consumption can cause systemic hypertension and

Safety and Toxicology

Vomiting, abdominal pain, photophobia, palpitations, muscle twitching, convulsions, miosis, and unconsciousness were described in several reports of nonfatal caffeine poisonings in children who ingested 80mgkg-1 caffeine. In several fatal accidental caffeine poisonings, cold chills, stomach cramps, tetanic spasms, and cyanosis were reported. The likely lethal dose in adult humans has been estimated to be approximately 10 g, which corresponds roughly to 150-200 mg kg-1. With daily doses of 110mgkg-1 given via intragastric cannula to female rats over 100 days, hypertrophy of organs such as the salivary gland, liver, heart, and kidneys was reported. Caffeine also induced thymic and testicular atrophy. Developmental and reproductive toxicity was associated with high, single daily doses of caffeine. The no-effect level for teratogenicity is 40 mg kg-1 caffeine per day in the rat, although delayed sternebral ossification can be observed at lower doses. This effect has been shown to be...

Clinical Description

FDCM DCM is a leading cause of heart failure and arrhythmia. Symptoms of congestive heart failure are dyspnea on exertion, decreased exercise tolerance, orthopnea, paroxysmal nocturnal dyspnea, fatigue, edema, and abdominal distension. Chest pain results from limited coronary vessel reserve. Ventricular arrhythmia leads to palpitations, syncope, and sudden cardiac death (SCD). Severe LV dilatation and dysfunction result in thrombo-embolic complications.

Clinical Features

Symptoms include atypical chest pain, palpitations, fatigue, and dyspnea unrelated to exertion. Symptoms are more common in those who know they have the syndrome. However, there is an increased incidence of sudden death and dysrhythmias in patients with MVP. There is also an increased incidence of transient ischemic attacks under the age of 45. In patients with MVP without mitral regurgitation at rest, exercise provokes mitral regurgitation in 32 percent of patients and predicts a higher risk for morbid events.5 The classic cardiac finding is a midsystolic click. The second heart sound may be diminished by the late systolic murmur, with crescendos into S2 (not present in all patients). Some patients may have pectus excavatum, a straight thoracic spine, or scoliosis. The ECG is usually normal, as is the chest radiograph unless the thoracic cage abnormalities described above are seen.

Hypertrophic Cardiomyopathy

CLINICAL FEATURES AND DIAGNOSIS Severity of symptoms in most instances is related to the patient's age the older the patient, the more severe the symptoms. Dyspnea on exertion is the most frequent initial complaint and is due to exercised-induced sinus tachycardia, which results in an abrupt elevated LV diastolic pressure and pulmonary venous hypertension. Additional symptoms include chest pain, palpitations, and syncope. A family history of death due to cardiac disease, frequently described as massive heart attack or heart failure, is not uncommon. Complaints of paroxysmal nocturnal dyspnea and pedal edema are infrequent. The HCM patient may be aware of forceful ventricular contraction and complain of an abnormal heartbeat or palpitations. Atrial and ventricular dysrhythmias are not uncommon in these patients rapid atrial dysrhythmias, especially atrial fibrillation, and particularly poorly tolerated because of the increased importance of the atrial contribution to LV filling in the...

TABLE 1016 Potential Complications of Tocolytic Agents

Subcutaneously and repeated hourly as needed until contractions stop, is commonly used. Common side effects include tachycardia, hypotension, palpitations, headaches, and tremor. Terbutaline should be withheld if the maternal pulse exceeds 140 beats per minute. The combination of magnesium sulfate and nifedipine is potentially dangerous, since nifedipine can enhance the toxicity of magnesium and result in neuromuscular blockade, interfering with both pulmonary and cardiac function. Careful monitoring of the mother and fetus with use of any of these agents, alone or in combination, is mandatory.

Emotional Processing

The neo-conditioning model proposes that the CS and UCS are cognitively represented, possibly in networks of interconnections among CSs, CRs, UCS, and UCR. The emotion processing model developed by Edna B. Foa and others (e.g., see Foa and Kozak, 1986) can be seen as an extension of the neo-conditioning model. According to the emotional processing model, fears are represented in networks known as fear structures stored in long-term memory. The networks contain cognitive representations of feared stimuli (e.g., oncoming trucks, driving at night), response information (e.g., palpitations, trembling, subjective fear, escape behaviors), and meaning information (e.g., the concept of danger). In the network the three types of information are linked (e.g., links between oncoming trucks, danger, and fear). Links can be innate (i.e., UCS-UCR links) or acquired by processes such as classical conditioning (CS-UCS links and CS-CR links). Fear structures are activated by incoming information that...

Reflexology In Disorders Of The Cardio Vascular System

PROBLEMS OF THE HEART Palpitations Angina pectoris The heart beats so silently that we are normally unaware of its working. Sometimes, however, it contracts so violently that the person is able to feel and or hear its beats. This condition is called palpitations. Usually, palpitations are not a symptom of a disease but merely a result of physical exercise or emotional excitement.

Shorttermeffects of estrogen deficiency

Hot flashes typically begin as the sudden sensation of heat centered on the face and upper chest, which rapidly becomes generalized. The sensation of heat lasts from two to four minutes, is often associated with profuse perspiration and occasionally palpitations, and is often followed by chills and shivering. Hot flashes usually occur several times per day.

Acute Exacerbations of COPD

Side effects of b2-adrenergic agonists include tremor, anxiety, and palpitations, so such agonists should be used with care in elderly patients known to have coexisting heart disease. PaO2 may fall slightly after use of these agents, due to pulmonary vasodilation and resultant ventilation-perfusion mismatch.

Investigation of syncope

The history is of paramount importance in the assessment of children ith syncope. Common but benign causes such as vasovagal syncope or hyperventilation are usually easily recognised. A history of syncope during or immediately after exertion, syncope preceded by palpitations, or syncope in the presence of a family history of premature sudden death, congenital long QT syndrome or hypertrophic cardiomyopathy should lead to referral for specialist evaluation. Detection of a cardiac murmur (or other abnormal signs on examination) should also lead to specialist referral as it may be a clue to the presence of aortic valve stenosis, coarctation of the aorta or hypertrophic cardiomyopathy.

Clinical Time Course Of Poisoning Routes Of Exposure

The time course and severity of the clinical effects of cyanide are a function of the nature of the cyanide-containing compound, the route of exposure, and the concentration of cyanide to which the patient is exposed. The onset of symptoms of poisoning following inhalational exposure to hydrogen cyanide gas is virtually immediate. Symptoms depend on the concentration of inspired gas. Several hours of exposure to low concentrations of gas (< 50 ppm) cause restlessness, anxiety, palpitations, dyspnea, and headache.12 Death may occur following prolonged exposure at these levels. Inhalational exposure to higher levels of hydrogen cyanide gas leads to severe dyspnea, loss of consciousness, seizures, and cardiac dysrhythmias. Coma, cardiovascular collapse, and death may occur immediately on exposure to very high levels. The LD50 for humans has been estimated at 200 ppm for a 30-min exposure and 680 ppm for a 5-min exposure.12

Katie M Castille and Maurice F Prout

A discrete period of intense fear or discomfort, in which at least four (or more) of the following symptoms developed abruptly and reached a peak within 10 minutes palpitations, pounding heart, or accelerated heart rate sweating trembling or shaking sensations of shortness of breath or smothering feeling of choking chest pain or discomfort nausea or abdominal distress feeling dizzy, unsteady, lightheaded, or faint derealization (feeling of unreality) or depersonal-ization (being detached from oneself) fear of dying pares-thesias (numbness or tingling sensations) and chills or hot flashes. Limited-symptom attacks require the same criteria, except that fewer than four symptoms of panic are required.

Clinical Manifestations

Clinical manifestations of hyperthyroidism reflect increased catabolism and excessive sympathetic activity caused by excess circulating thyroid hormones. Symptomatic manifestations of hyperthyroidism include weight loss despite normal or increased appetite, heat intolerance, anxiety, irritability, fatigue, muscle weakness, palpitations, and oligomenorrhea. Signs of hyperthyroidism include goiter, tremor, hyperreflexia, fine or thinning hair, thyroid bruit, muscle wasting, and cardiac arrhythmias such as sinus tachycardia or atrial fibrillation. The presentation of hyperthyroidism varies with age. Young patients typically present with hypermetabolism, while older patients may present primarily with tachyarrhythmias or cardiac failure. Rarely, elderly patients experience only muscle wasting, apathy, confusion, or a state of depression known as apathetic hyperthyroidism. Clinical features of hypothyroidism include cold intolerance weight gain constipation edema of the hands, feet, and...

TABLE 2061 Causes of Thyrotoxicosis

Classically, patients with hyperthyroidism may complain of heat intolerance, palpitations, weight loss, sweating, tremor, nervousness, weakness, and fatigue ( Table 2.0.6-2). An individual with hyperthyroidism who is exhibiting only mild symptoms may be safely referred for further evaluation as an outpatient. Clinical suspicion of hyperthyroidism is confirmed by thyroid function tests. An elevated free T4 and a low or undetectable TSH level is consistent with a diagnosis of hyperthyroidism. In some cases of Graves' disease, the T4 level may be normal and the TSH level decreased but the patient appears to be thyrotoxic. A T 3 level should be determined to rule out T3 toxicosis. Patients with hyperthyroidism secondary to pituitary adenomas will have elevated TSH.

Differential Diagnosis

Carcinoma of the thyroid, pheochromocytoma, and primary hyperparathyroidism. Serum calcitonin levels serve as a useful tumor marker for medullary carcinoma of the thyroid. A history of headaches, excessive sweating, tachycardia, palpitations, or hypertension should alert the clinician about the possibility of an associated pheochromocytoma. Measurement of 24-hour urinary levels of catecholamines, metanephrines, and vanillylmandelic acid is the best screening test for pheochromocytoma.

Theoretical Bases

The major contemporary theory of fears is E. B. Foa and M. J. Kozak's 1986 emotional processing model. Here, fears are represented in networks (fear structures) stored in long-term memory. The networks contain representations of feared stimuli (e.g., oncoming trucks, driving at night), response information (e.g., palpitations, trembling, subjective fear, escape behaviors), and meaning information (e.g., the concept of danger). In the network the three types of information are linked (e.g., links between oncoming trucks, danger, and fear). Links can be innate or learned. Fear structures are activated by incoming information that matches information stored in the network. Activation of the network evokes fear and motivates avoidance or escape behavior. According to this model, fears are reduced by modifying the fear structure through the incorporation of corrective information (e.g., safety information acquired durign behavioral exposure exercises). Although the emotional processing...

Clinical Features Acute Overdose

The signs and symptoms of MAOI toxicity are often nonspecific. Even in its most severe form, it can resemble numerous other conditions (see below). Most clinical overdose information has come from single case reports or case series, with tremendous variation in presentation. Hence, there is no typical presentation to MAOI toxicity nor is there an orderly progression of symptoms. The clinician should anticipate the rapid development of life-threatening symptoms in all MAOI overdose patients. The initial symptoms of MAOI overdose are reported to include headache, agitation, irritability, nausea, palpitations, and tremor. The earliest signs of MAOI toxicity include sinus tachycardia, hyperreflexia, hyperactivity, fasciculations, mydriasis, hyperventilation, nystagmus, and generalized flushing. In cases of moderate toxicity, opisthotonus, muscle rigidity, diaphoresis, chest pain, hypertension, diarrhea, hallucinations, combativeness, confusion, marked hyperthermia, and trismus may become...

Betaadrenergic receptor agonists

Maternal side effects include tachycardia, palpitations, and lowered blood pressure. Myocardial ischemia is rare. Common side effects include chest discomfort (10 percent), shortness of breath (15 percent), palpitations (18 percent), tremor (39 percent) and anxiety. Pulmonary edema is an uncommon maternal complication, occurring in 0.3 percent.

Solid Renal and Juxtarenal Lesions

Vincristine Syringe

Because of their biologically active nature, neuro-blastomas may secrete a significant amount of cate-cholamines and hence, patients may present with palpitations, tachycardia, hypertension, flushing, and sweating. Intractable diarrhea may result from the secretion of vasoactive intestinal peptide (VIP) (Gesundheit et al. 2004). Another unusual symptom is cerebel-lar ataxia and opsomyoclonus (dancing feet, dancing eyes myoclonic encephalopathy of infants). This syndrome is rare, of unknown etiology, and is usually associated with thoracic lesions (Bousvaros et al. 1986). Malaise, pain, and anemia may be the presenting complaint in up to 60 secondary to metastatic disease.

TABLE 2022 Frequency of Presenting Signs and Symptoms in Hypoglycemia

A rapid fall in blood glucose levels or the hypothalamic sensing of neuroglycopenia causes the release of the counterregulatory hormones, primarily the catecholamines epinephrine and norepinephrine. The release of the latter is responsible for the hyperepinephrinemic findings, including anxiety, nervousness, irritability, nausea, vomiting, palpitations, and tremor. Such signs and symptoms were noted in 8 percent of ED patients with hypoglycemia. 4

Neuroglycopenic Syndromes

This syndrome comprises a collection of vague symptoms such as feelings of alternating hot and cold, feeling unwell, anxiety, panic, inner trembling, unnatural feelings, blurring of vision, and palpitations, any or all of which may be accompanied by objective signs of facial flushing, sweating, tachycardia, and unsteadiness of gait. There is no particular order in which these features occur, nor are they constant. Nevertheless, patients on insulin therapy for diabetes, in whom they are common, rely upon them to warn of more severe neuroglycopenic impairment culminating in loss of consciousness. These patients can be taught to abort progression of symptoms by eating carbohydrate.

TABLE 241 Common Dysrhythmias of Digoxin Toxicity Approximate Incidence

SVT often causes a sensation of palpitations and light-headedness. In patients with coronary artery disease, anginal chest pain and dyspnea may occur from the rapid heart rate. Frank heart failure and pulmonary edema may occur in patients with poor left ventricular function. The decrease in diastolic filling period and subsequent decrease in cardiac output cannot be tolerated in the patient with left ventricular failure.

Habituation and Extinction Models

Still another explanation is that the context determines which meaning a situation becomes. It has been suggested that the joint presence of the stimulus (e.g., palpitations) and the context (e.g., far from home) determine the meaning (e.g., heart attack). The latter theory is in line with evidence that return of fear may be minimized with prolonged exposure sessions to a variety of contexts.

Diagnosis of Cobalamin Deficiency

Cobalamin deficiency is suspected in individuals who display the typical manifestations of deficiency of the vitamin as described in the section above on the effects of deficiency. In addition to the symptoms that may be experienced by individuals that are related to anemia (easy fatigue, shortness of breath, palpitations) and neuropathy (sensory and motor disturbances and memory loss) there are features that may be detected by a physician, including skin pallor (from anemia), abnormalities in neurological examination (sensory loss, abnormal balance and reflexes, mental changes), and epithelial changes (skin pigmentation, smooth tongue). On the basis of any combination of such changes, cobalamin

Adrenal Incidentaloma

Obtaining a thorough history and physical examination should be the first step in evaluating the patient found to have an adrenal incidentaloma. Functional tumors, primary adrenocortical cancers, or metastases to the adrenal gland can often be diagnosed on the basis of a detailed history and physical examination alone. Questions should therefore be directed to rule out these entities. The patients should be asked about excessive weakness, extremes of mood, or recent unexplained weight changes. Females should be asked about a deepening of their voice, recent growth of hair on their face, chest, or arms, or changes in menstruation. Likewise, males should be questioned about breast enlargement or impotence. All of these questions are directed at identifying benign or malignant functioning adrenocortical tumors that can secrete steroid hormones such as cortisone, aldosterone, or sex hormones. In addition, the presence of symptoms associated with a pheochromocytoma, such as hypertension,...

Prediction of SCD

It is necessary to accurately predict who is at risk for SCD for any prevention strategy to be of value. Unfortunately, the majority of future SCD victims cannot be identified in advance. Prodromal symptoms in the days to weeks preceding cardiac arrest are common but usually too nonspecific to be of important predictive value. In one of the largest series in which survivors of SCD were questioned about events preceding their collapse, Goldstein et al. 20 found that 71 percent of SCD survivors reported no prodromal symptoms or symptoms of 1 h or less in duration. Prodromal symptoms were present for more than 1 h in only 29 percent of patients. The most common symptoms reported by SCD survivors or family members of SCD victims are chest pain, dyspnea, and palpitations.

Adrenergic Agents

The most common side effect of b-adrenergic drugs is skeletal muscle tremor. Patients may also experience nervousness, anxiety, insomnia, headache, hyperglycemia, palpitations, tachycardia, and hypertension. Despite earlier concerns over potential cardiotoxicity, especially when these drugs were used in combination with theophylline, clinical experience has not revealed significant problems. Arrhythmias and evidence of myocardial ischemia are rare, especially in patients without prior history of coronary artery disease.


Up to 45 percent of insulin-dependent diabetics will require evaluation for severe hypoglycemia at some time during the course of their pregnancy. 2 Hypoglycemia generally presents as sweating, tremors, blurred or double vision, weakness, hunger, confusion, paraesthesias, anxiety, palpitations, nausea, headache, or stupor. Hypoglycemic episodes are generally well tolerated by the fetus. Mild hypoglycemia that is, a glucose < 70 mg dL in a patient who is able to follow commands can be treated by administration of one cup of low-fat milk together with bread or crackers every 15 min. This regimen is preferred over more highly concentrated glucose solutions because it avoids overshoot and subsequent hyperglycemia. In patients who are unable to cooperate with oral therapy owing to severe hypoglycemia, parenteral therapy may be begun using one ampule (50 mL) of a 50 percent dextrose solution given via intravenous push. Alternatively, the patient may be treated using glucagon 1 to 2 mg IM...


Hypoglycemia may be an end product of an endocrinopathy (e.g., adrenal insufficiency, hyperthyroidism, or hypopituitarism) or the result of an exogenous substance, such as ethanol, salicylate, oral hypoglycemics, and insulin. Hypoglycemia may result from a common stress pathway of decreased gluconeogenesis, as seen during sepsis or Reye syndrome. Adrenergic signs of palpitations, hunger, and sweating are seen at levels less than 60 mg dL. Irritability, confusion, seizures, and coma occur at levels of 40 mg dL or less. Infants and children are prone to develop ketotic hypoglycemia with fasting, especially with infections in early infancy. AMS from hyperglycemia is rare in children. The most common cause of hyperosmolar central nervous system dysfunction is diabetic ketoacidosis.

Ischemic Equivalents

Because of the visceral afferent innervation of the myocardium as well as the many confounding factors affecting the perception of ischemia, many patients with ACS will not experience chest discomfort. Up to one-third of AMIs may be silent, occurring without any reports of symptoms from the patient and discovered incidentally on routine ECG.1 Many other patients present with ischemic-equivalent symptoms, which may include one or any combination of the following dyspnea at rest or exertion shoulder, arm, or jaw discomfort epigastric discomfort nausea light-headedness generalized weakness acute changes in mental status or diaphoresis. Other atypical features associated with ischemia, particularly in women, include repetitive chest pain, pain relieved by antacids, pain unrelated to exercise, pain not relieved with rest or nitoglycerin, or palpitations without chest pain. 2 Upper abdominal discomfort, despite relief with antacids, can also be a symptom of myocardial ischemia for patients...

Justina C Wu MD PhD

Echocardiography Images

An 80-yr-old male with a history of hypertension who presented with acute onset of chest pain associated with mild shortness of breath and palpitations, lasting a total of 20 min by the time he was transported to the hospital. On physical exam he appeared uncomfortable, diaphoretic, tachycardic, and with a blood pressure of 90 60 mmHg. Lungs were clear to auscultation, and a cardiac exam revealed an S3 without murmurs or rub. His electrocardiogram (ECG) displayed 5-mm ST elevations in leads V1-5 with lesser elevations in the inferior leads, and the initial chest X-ray showed clear lungs. Cardiac enzymes were sent, and the patient started on aspirin and heparin in addition to lytic therapy with Retavase .

Clinical History

The symptoms of ischemic heart disease that should be sought and characterized include chest discomfort, severity, location, radiation, duration, and quality. In addition, the presence of associated symptoms such as nausea, vomiting, diaphoresis, dyspnea, light-headedness, syncope, and palpitations may be helpful. A detailed history regarding the onset and duration of symptoms, activities that precipitate symptoms, and prior evaluations for similar symptoms should be ascertained. Cardiac risk-factor assessment should be performed.

Case Presentation

J.R. is an 83-yr-old Caucasian man with a long history of hypertension treated with diuretics and an angiotensin converting enzyme inhibitor. One week before presentation, he noted the onset of increasing fatigue and occasional palpitations when walking briskly to his office. He has been able to continue working full-time in his optometric office, but for the past 2 d, has noted new pedal edema. Last night, he had an episode of paroxysmal nocturnal dyspnea. At presentation to his internist, he is found to be in mild respiratory distress with a respiratory rate of 18 min. Blood pressure is 164 86 mmHg bilaterally, heart rate 120 bpm, irregularly irregular. There is mild jugular venous distension. Carotids are brisk without bruits. Lung exam demonstrates bibasilar rales. His point of maximal impulse is in the fifth intercostal space, anterior axillary line. There is a normal S1, S2 with II VI holosystolic murmur best heard at the apex in the left lateral


Fatigue, palpitations, light-headedness, and lack of energy. Oral manifestations include angular cheilitis, diffuse or patchy atrophic glossitis, and mucosal atrophy. Associated oral candidiasis is common. Such oral changes are rarely seen in the developed world because iron-deficiency anemia is identified relatively early. 19

Sick sinus syndrome

In addition to the effect of pacing mode on the incidence of atrial fibrillation, atrial rate and pacing site can also have an important impact on atrial arrhythmias. Overdrive pacing is routinely used following cardiac surgery to prevent postoperative atrial fibrillation. Similarly, higher base pacing rates are often employed in patients with paroxysmal atrial fibrillation to inhibit tachyarrhythmias, although the utility of this strategy is not well documented. In fact a recent study comparing maintaining atrioventricular synchrony with no atrial pacing (VDD mode) and frequent dual chamber pacing (DDDR mode) showed no difference in the frequency of atrial fibrillation.6 The potential disadvantages of atrial overdrive pacing include decreased pulse generator longevity and the development of palpitations and insomnia if constant rapid rates are used. In an effort to avoid rapid overdrive pacing, several algorithms are being tested that periodically sample the intrinsic heart rate and...

Fast Cardiac Rates

SUPRAVENTRICULAR TACHYCARDIA This is the most common dysrhythmia in the pediatric age range. In infants, SVT presents with a 4- to 24-h history of poor feeding, tachypnea, pallor, and lethargy. In older children, palpitations and chest pain can be prominent in the symptomatology. Physical examination reveals weak pulses and a tachycardia that can be too rapid to be counted accurately. Depending on the time since onset of SVT, other physical signs can vary from congestive heart failure to cardiogenic shock with pending arrest. Low cardiac output is secondary to inadequate ventricular diastolic filling time.

Tyramine Reaction

The tyramine reaction is typically of rapid onset, occurring within 15 to 90 min after the dietary amine is ingested. The severity of this reaction is highly variable and partially related to the total amount of tyramine ingested. The hallmark symptom of the tyramine reaction is a severe occipital or temporal headache. Other associated symptoms include hypertension, diaphoresis, mydriasis, neck stiffness, pallor, neuromuscular excitation, palpitations, and or chest pain. Most symptoms gradually resolve over 6 h without specific therapy but fatalities have been rarely reported, usually due to intracranial hemorrhage or myocardial infarction. Therefore, an electrocardiogram should be obtained on all patients with tyramine-associated chest pain. Focal neurologic findings or a persistent severe headache warrants investigation with a computed tomography (CT) scan of the head.


Pheochromocytomas account for approximately 0.1-1 of hypertensive patients. While hypertension is the most common clinical feature of a pheochromocytoma, hypertension may be episodic in one third of patients and absent in one fifth.17 In a hypertensive patient, the triad of paroxysms of headache, palpitations and sweating is classic but not diagnostic because the prevalence in this group of patients is only 5.9 .18 The clinical picture, however, may be obscure. A significant proportion of patients may present with atypical symptoms including anxiety, tremulousness, abdominal pain and vomiting, weight loss, visual disturbances, shortness of breath or cardiac failure. The initial finding may be the consequence of hypertension such as a myocardial infarction or stroke.19,20 For some patients with pure epinephrine-producing tumors the initial presentation may be hypotension or shock due to epinephrine-mediated peripheral vascular dilation.21 Death from unsuspected pheochromocytomas is not...


SIDE EFFECTS AND CONTRAINDICATIONS The common side effects of flushing, headache, pedal and periorbital edema formation, and palpitations are relatively well tolerated. The less common, but more serious, complications that have occurred include cerebral ischemia, syncope, complete heart block, symptomatic hypotension, sinus arrest, retinal ischemia, congestive heart failure, and myocardial ischemia infarction. Rebound hypertension can also occur when nifedipine therapy is stopped abruptly.