Tachycardia, like dyspnea, is usually a sign that the tissues are not getting enough oxygen to meet their demands. To recall a list of causes, pathophysiology is applied. If tachycardia results from anoxia, then the causes can be developed on the basis of the causes for anoxia, which may result from a decreased intake of oxygen, a decreased absorption of oxygen, and inadequate transport of oxygen to the tissues. Tachycardia also results when the tissues’ demand for oxygen increases. Another cause is peripheral arteriovenous shunts. In addition, anything that stimulates the heart directly, such as drugs, electrolyte imbalances, or disturbances in the cardiac conduction system, will cause tachycardia. Let us review the conditions that may fall into each of these categories.

  • Decreased intake of oxygen: Anything that obstructs the airway and prevents oxygen from getting to the alveoli should be recalled in this category. Bronchial asthma, laryngotracheitis, chronic bronchitis, and emphysema are most important to recall. In addition, if the “respiratory” pump (thoracic cage, intercostal and diaphragmatic muscles, and respiratory centers in the brainstem) is affected by disease, especially acutely, there will be tachycardia. Poliomyelitis, myasthenia gravis, barbiturate intoxication, and intoxication by other central nervous system (CNS) depressants are examples of disorders in this category. Finally, the intake of oxygen may decrease if there is a low atmospheric oxygen tension. High altitude is an obvious cause, but hazardous working conditions must also be considered.

  • Decreased oxygen absorption: This may result from three mechanisms.

    • Alveolar–capillary block in sarcoidosis, pneumoconiosis, pulmonary fibrosis, congestive heart failure (CHF), alveolar proteinosis, and shock lung.

    • Diminished perfusion of the pulmonary capillaries in pulmonary emboli and pulmonary and cardiovascular arteriovenous shunts.

    • Disturbed ventilation/perfusion ratio in which alveoli are perfused but not well ventilated, in alveoli that are not well ventilated, or in alveoli that are ventilated but not well perfused. This is typical of pulmonary emphysema, atelectasis, and many chronic pulmonary diseases.

  • Inadequate oxygen transport: Severe anemia, shock, and CHF (regardless of the cause) fall into this category, as do methemoglobinemia and sulfhemoglobinemia.

  • Increased tissue oxygen demands: Fever, hyperthyroidism, leukemia, metastatic malignancies, polycythemia, and certain physical or emotional demands fall into this category.

  • Peripheral arteriovenous shunts: These shunts may occur in the popliteal fossa following a gunshot wound, in the sellar area following the rupture of a carotid aneurysm into the cavernous sinus, and in Paget disease.

  • Disorders that directly affect the heart: Stimulants of the heart such as caffeine, adrenalin (pheochromocytomas), thyroid hormone (hyperthyroidism), amphetamines, theophylline, and other drugs fall into this category. Nervous tension and neurocirculatory asthenia may be the cause. Electrolyte disturbances such as hypocalcemia and hypokalemia may precipitate ventricular tachycardia. Excessive amounts of digitalis may also provoke atrial or ventricular tachycardia.

Tachycardia of various types may occur from disturbances in the conducting system of the heart. Digitalis has already been mentioned, but the Wolff–Parkinson–White syndrome, focal myocardial anoxia from emboli or infarction, and distention of various chambers of the heart (atria in mitral stenosis, ventricles in essential hypertension and cor pulmonale) are also etiologies of this mechanism. Anticholinergic drugs such as atropine block the ability of the vagus to slow the heart and may cause or contribute to tachycardia. All of the above categories are outlined in Table 56 where a few diseases that are more specific are mentioned.

Approach to the Diagnosis

The association of other clinical signs and symptoms will often help to pinpoint the diagnosis. Tachycardia with tremor and an enlarged thyroid suggests hyperthyroidism. Tachycardia with respiratory wheezes suggests bronchial asthma. Tachycardia with a black stool suggests a bleeding peptic ulcer. If the blood pressure is low, the workup will proceed as that of shock (see page 253). In contrast, tachycardia with a normal blood pressure should prompt thyroid function studies, pulmonary function studies, arterial blood gases, and a venous pressure and circulation time. Electrolyte determinations, a drug screen, and 24-hour urine for catecholamine determinations may be indicated if there is hypertension as well.

Other Useful Tests

  • Complete blood count (CBC) (anemia)

  • Sedimentation rate (infection)

  • Chemistry panel (liver disease, uremia)

  • Antinuclear antigen (ANA) (collagen)

  • Antistreptolysin O (ASO) titer (rheumatic fever)

  • Blood cultures (subacute bacterial endocarditis [SBE])

  • Febrile agglutinins (fever of unknown origin)

  • Serial electrocardiograms (ECGs) and cardiac enzymes (myocardial infarction)

    Table 56 Tachycardia

    Allergic and Autoimmune
    Decreased Intake of Oxygen Aortic aneurysm with compression of bronchi Laryngitis
    Carcinoma of the lung Pulmonary emphysema Pneumoconiosis α1-Trypsin deficiency
    Cystic fibrosis
    Bronchial asthma Pneumothorax  
    Increased Oxygen Absorption Pulmonary embolism Pneumonia Hemangioma
    Carcinoma of the lung
    Pulmonary emphysema
    Shock lung
    Lipoid pneumonia
    Congenital cyst Scleroderma
    Wegener granulomatosis
    Shock lung Fat emboli
    Inadequate Oxygen Transport Shock from myocardial infarction
    Congestive heart failure
    Septicemic shock   Aplastic anemia Drug-induced shock
    Sickle cell anemia
    Cooley anemia
    Hemolytic anemia (autoimmune) Hemorrhagic shock  
    Peripheral Arteriovenous Shunts       Paget disease   Carotic–cavernous shunt   Popliteal aneurysm  
    Increased Tissue Demands for Oxygen   Septicemia
    Fever of any infection
    Hodgkin lymphoma
    Polycythemia vera
    Disorders Affecting the Heart Directly Myocardial infarction
    Essential hypertension
    Rhabdomyosarcoma Muscular dystrophy Caffeine
    Wolff–Parkinson–White syndrome
    Glycogen storage disease
    Lupus erythematosus Traumatic aneurysm Hyperthyroidism


  • Lung scan (pulmonary embolism)

  • Holter monitoring (cardiac arrhythmia)

  • Echocardiography (CHF, valvular heart disease)

  • 5-hour glucose tolerance test (insulinoma)

  • Temperature chart (fever of unknown origin)

  • Sleeping pulse rate (anxiety neurosis)

  • Psychiatric consult

Taste Abnormalities

The causes of taste abnormalities can be recalled simply by visualizing the various structures around the tongue, mainly the nose, throat, teeth, gums, joints, and nerves. It is wise to start our discussion with the tongue.

  • Tongue—Glossitis, stomatitis

  • Nose—Rhinitis, sinusitis, and hay fever

  • Throat—Tonsillitis and pharyngitis

  • Teeth—Dental cases, alveolar abscess

  • Gums—Gingivitis

  • Joints—Temporomandibular joint syndrome

  • Nerves—Bell palsy, brainstem lesions, uncinate fits (epilepsy)

Unfortunately, this method would fail to help recall the drugs and poisons that cause taste abnormalities such as penicillamine, bismuth, iodine, bromide, and mercury.

Approach to the Diagnosis

Careful examination of the nose and throat ought to reveal most of the above conditions. A neurologic examination should reveal Bell palsy and brainstem lesions. X-ray of the teeth will demonstrate dental cases and abscess. A wake-and-sleep electroencephalogram (EEG) with nasopharyngeal electrodes will be necessary to diagnose uncinate fits. Laboratory studies include a urine drug screen, CBC, chemistry panel, and venereal disease research laboratory (VDRL) test. A psychiatrist should be consulted if there are no objective findings and these studies are negative.

Testicular Atrophy

The causes of this sign can best be recalled by using the mnemonic VINDICATE.

  • V—Vascular conditions bring to mind varicoceles, which cause atrophy on the side of the dilated veins.

  • I—Inflammation recalls the atrophy following mumps, orchitis, and other causes of epididymo-orchitis.

  • N—Neoplasms suggest the atrophy that occurs in the estrogen treatment of prostatic carcinoma.

  • D—Degenerative disorders suggest the atrophy resulting from aging.

  • I—Intoxication should remind one of the atrophy resulting from chronic alcoholism, Laennec cirrhosis, and hemochromatosis. X-ray exposure may also produce atrophy.

  • C—Congenital disorders recall undescended testes and torsion.

  • A—Autoimmune and allergic disorders suggest nothing.

  • T—Trauma reminds one of the atrophy following vasectomy and accidental ligation of the blood supply during hernia repair.

  • E—Endocrine disorders suggest the atrophy of hypopituitarism, Klinefelter syndrome, and other eunuchoidal states.

Approach to the Diagnosis

The workup of testicular atrophy may require a chromatin analysis, serum testosterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels, and biopsy, but referral to an endocrinologist is the best way to get this accomplished with accuracy.

Other Useful Tests

  • Sperm count

  • VDRL (syphilis)

  • Serum iron and iron-binding capacity (hemochromatosis)

  • Liver biopsy (hemochromatosis)

  • Electromyogram (EMG) (myotonic dystrophy)

  • Urology consult

  • Computed tomography (CT) scan of the brain (pituitary insufficiency)

Testicular Mass

Like that of most masses, the differential diagnosis of testicular masses is best analyzed by the anatomic and histologic approach (Table 57). The skin may be involved by many inflammatory conditions leading to swelling, including carbuncles, cellulitis, and dermatitis of various types. Edema of the skin and subcutaneous tissue is found in cirrhosis, CHF, nephrosis, and filariasis. The tunica vaginalis is involved with hernias and hydroceles, which may be differentiated by using transillumination. The venous plexus of the scrotum and testes is involved by varicoceles and phlebitis (usually of the left venous plexus), and a varicocele may be the sign of a carcinoma of the kidney when the left spermatic vein is obstructed. Thus, one readily sees how frequently obstruction is a pathophysiologic mechanism in tumors here or elsewhere.

The testis is swollen in carcinomas (e.g., seminomas, choriocarcinomas, teratomas, Leydig cell tumors) and in orchitis (secondary to mumps, bacterial diseases, syphilis, or tuberculosis). The epididymis is frequently inflamed and swollen when there is orchitis and only rarely is inflamed by itself. It may also be enlarged from a spermatocele or from a vas deferens obstruction caused by prostatic disease (inflammation or neoplasm). Finally, arterial occlusion caused by torsion of the testicle may cause a testicular mass.

Approach to the Diagnosis

Testicular masses may be differentiated by transillumination (hydroceles and spermatoceles transilluminate, whereas hernias and tumors do not). Hernias may also be differentiated by reducing them (some will not reduce,

however, if they are incarcerated), and auscultation may reveal bowel sounds. In noncommunicating hydroceles and testicular tumors, one may get above the swelling, whereas in torsion and hernias one cannot. In torsion, the tenderness is decreased by elevation of the testicle, whereas in orchitis the tenderness is not relieved unless elevation is done for an hour or more. Ultrasonography will easily distinguish between torsion and orchitis because of the significant decrease in blood supply to the testicle in torsion. Serum α-fetoprotein β-human chorionic gonadotropin (HCG) or lactic dehydrogenase (LDH) will be elevated in testicular tumors. Surgery may be the only way to differentiate the cause of the mass.

Testicular atrophy.

Testicular mass.

Sep 23, 2018 | Posted by in CRITICAL CARE | Comments Off on T

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