Articles on Medical Diseases and Conditions

Month: October 2009

  • Antiarrhythmic medications

    Antiarrhythmic medications  slow down rapid heartbeats  and regulate irregular or premature heartbeats. Generally, these drugs work by block- ing chemical reactions that promote  electrical conduction.  They act to either suppress abnormal electrical impulses or slow down transmission of impulses as they are conducted through  heart tissue. As a result, your heart beats more rhythmically and you experience fewer symptoms.

    You may be given these medications  intravenously  during an emergency situation, or they may be prescribed for you to take orally for an inde?nite  period.  Certain  antiarrhythmics, such as amiodarone,  cause side effects such as increased sensitivity to sunlight. This drug may also affect your vision, the thyroid, or the lungs. Many people are surprised to learn that an antiarrhythmic drug can in fact cause an arrhythmia or make an existing one more frequent or more severe.

    You and your doctor  will need to carefully consider  the balance of bene?ts and risks of medication. Your doctor will also do thorough test- ing and monitoring, either with Holter monitoring, electrophysiologic studies, or both, to determine what drug works best for you. The electrophysiologic  testing  indicates  how well a medication  is controlling your symptoms, exactly how it alters your heart’s rhythm, and how well it protects your heart from an arrhythmia induced during the study.

    Apart  from  these  antiarrhythmics, medications  such  as calcium channel blockers  or beta-blockers   may be prescribed.

    If you have atrial ?brillation,  which can make you more susceptible to blood clots, you will probably  also take an anticoagulant or an antiplatelet  medication  . As with all medica- tions, drug interactions  with antiarrhythmics are always a concern;  be sure to let your doctor  know about other  medications  you are taking, including over-the-counter drugs and herbal remedies.

  • Blood Oxygen Studies

    The greatest stimulus for arterial as opposed to venous specimens for blood gas studies is to obtain measurement of blood oxygen. The usual information reported is PO2 (concentration of O2 gas measured in mm of Hg or Torr), obtained with a direct-reading PO2 electrode. PO2 represents the dissolved oxygen content of plasma, analogous to the relationship of PCO2 to CO2. Reference ranges for PO2 are age related. In persons under age 60 (breathing room air), 80-95 mm Hg is considered normal. Over age 60, 1 mm Hg per year, but no more than 20 mm Hg, is subtracted from the lower limit of the reference range. A PO2 of 60-80 mm Hg is classified as mild hypoxemia, a PO2 of 40-60 mm Hg represents moderate hypoxemia, and a PO2 less than 40 mm Hg represents severe hypoxemia.

    Blood oxygen studies are done for three reasons. First, they help indicate the current status of alveolar gas exchange with inspired air. PO2 provides this information. A normal PO2 while breathing room air indicates adequate pulmonary ventilation.

    The second reason is to determine the amount of oxygen available to body cells. PO2 is less adequate for this purpose, because most of the oxygen in the blood is not dissolved oxygen but oxygen bound to RBC hemoglobin. The measurement one really needs is oxygen saturation, which is the actual amount of oxygen bound to hemoglobin compared with the theoretical amount that should be bound to the same amount of hemoglobin (or, the amount of hemoglobin bound to oxygen compared to the amount of hemoglobin available for binding). Then, the quantity of hemoglobin times percent saturation times the factor 1.34 gives the total quantity of oxygen in the blood (except for the very small amount of dissolved oxygen). When the hemoglobin level is normal and PO2 is normal, the percent saturation and total oxygen content are usually adequate. In fact, many blood gas machines provide a calculated oxygen saturation value derived from PO2, normal hemoglobin levels, and data from the normal oxgyen-hemoglobin dissociation curve. Although there is adequate correlation between calculated oxygen saturation and actual (true) oxygen saturation (measured in a special instrument such as a CO-Oximeter) at normal hemoglobin and PO2 values, calculated O2 saturation results can become significantly incorrect at subnormal PO2 values, due to the sigmoid (S) shape of the oxygen-hemoglobin dissociation curve. In the steep midportion of the S curve, a relatively small decrease in PO2 leads to a relatively large decrease in oxygen saturation. In addition, there are a considerable number of conditions that shift the curve to greater or lesser degree and affect oxygen saturation. Nevertheless, a decreased PO2 suggests the possibility of tissue hypoxia, and the degree of PO2 decrease provides a rough estimate of the probability and severity of tissue hypoxia. Certain conditions decrease blood oxygen content or tissue oxygen independently of PO2. These include anemia (producing decreased hemoglobin and therefore decreased oxygen-carrying capacity), carbon monoxide poisoning (CO replaces O2 on the hemoglobin molecule), acidosis (which increases oxygen dissociation from hemoglobin), and congestive heart failure (which slows blood flow and decreases tissue perfusion rate). Hemoglobins that do not carry oxygen (e.g., Hb F), if present in sufficient quantity, result in decreased O2 saturation values.

    The third reason for PO2 measurement is to monitor effects of oxygen therapy. The usual goal is to raise PO2 above the lower limit of the reference range. However, in some patients, oxygen therapy may be adequate but unable to provide a normal PO2.

    Oxygen saturation (SaO2) is another frequently used parameter of tissue oxygenation. This is a measurement of arterial blood oxygen content. As discussed previously, SaO2 can be measured directly by an instrument called a CO-oximeter or estimated by calculation from PO2 and hemoglobin quantity; it can also be measured indirectly by means of a pulse oximeter (discussed later).

  • Anion Gap

    Once metabolic acidosis is apparent, the problem becomes one of identifying the cause. Calculation of the anion gap may be helpful. The anion gap is the difference between the major cations (sodium, or sodium plus potassium) and the major anions (chloride and bicarbonate). The anion gap formula is: AG = Na – (C1 + HCO–3). If the anion gap is increased, and especially when it is more than 10 mEq/L above the upper limit of the reference range, excess organic acids or acidic foreign substances should be suspected. Conditions in which these may appear include diabetic ketoacidosis, ethyl alcohol-induced ketoacidosis, renal failure, lactic acidosis, salicylate overdose, and methanol or ethylene glycol poisoning. The value most often listed for normal anion gap is 8-16 mEq/L (mmol/L). However, there is some disagreement in the literature whether to use a range of 8-12 or 8-16 mEq/L for a normal anion gap. Some investigators use the sum of sodium plus potassium in the equation rather than sodium alone. Although one would expect this to decrease the normal anion gap, the reference values reported in the literature are the same or even greater than those for the formula using sodium alone, with some listing a range of 8-16 mEq/L and others 8-20 (values in the literature can be found extending from 7-25 mEq/L). Anion gap reference ranges established on hospitalized patients tend to be higher than those established on outpatients. A collection tube filled to less than one third of tube capacity can result in a falsely decreased bicarbonate and falsely increased anion gap.

    A decreased anion gap has been associated with multiple myeloma. However, one report indicates that most calculated anion gaps that are decreased result from laboratory error in test results included in the equation, with hypoalbuminemia and hyponatremia the next most common associated findings.

  • Other Comments on Acid-Base Problems

    The preceding discussion applies to an acid-base problem involving a single primary metabolic or primary respiratory abnormality, with or without body attempts at compensation. Unfortunately, in some cases the laboratory picture is more complicated; for example, when there are superimposed attempts at therapy or when two different acid-base processes coexist (referred to as “mixed acid-base disorders”). An example is diabetic acidosis (metabolic acidosis) in a patient with chronic lung disease (compensated respiratory acidosis). In this circumstance it is very important to decide what serious clinical condition the patient has (e.g., renal failure, diabetic acidosis, chronic lung disease) that might affect the acid-base status and then what other conditions may be superimposed (such as vomiting, diuretic therapy, or shock) that could alter the acid-base picture in a certain direction.

    PCO2 Values in Metabolic and Respiratory Acid-Base Disorders
    PCO2 NORMAL
    An abnormality in pH means an uncompensated metabolic process.
    PCO2 ABNORMAL
    PCO2 decreased
    Could be respiratory (hyperventilation) in origin (respiratory alkalosis). If so, pH should be increased (acute onset), or normal, but more than 7.40 (chronic-compensated).
    Could be metabolic acidosis. If so, pH should be decreased (partial compensation), or normal but more than 7.40 (fully compensated).
    PCO2 increased:
    Could be respiratory (hypoventilation) in origin (respiratory acidosis). If so, pH should be decreased (acute onset), or normal but less than 7.40 (chronic-compensated).
    Could be metabolic alkalosis. If so, pH should be increased (partial compensation), or normal, but more than 7.40 (fully compensated).

    In some cases of acid-base disturbance, such as classic diabetic acidosis, the diagnosis may be obvious. In other cases the diagnosis is made from the first set of arterial blood gas measurements. In these two situations, continued acid-base studies are needed only to gauge the severity of the disorder and response to therapy. If the PO2 does not indicate respiratory impairment, it may be sufficient to obtain PCO2 or HCO3 values, with or without pH determination, on venous specimens rather than make repeated arterial punctures.

  • Diagnosing Arrhythmias

    Once your doctor diagnoses an arrhythmia through your symptoms or an examination, he or she will need to determine where it originates and whether it requires treatment; that is, whether it is causing symptoms or putting  you at risk for more serious problems in the future.

    The electrocardiogram  is a very important tool that  your  doctor  uses to  diagnose  and  study  your  arrhythmia. The ECG  records and measures the path and timing of your heart’s electri- cal impulses from their origin in the sinoatrial node, through the atria, through the atrioventricular node, and into and through the ventricles. However,  the  standard  ECG  can only  record  the  electrical  activity that takes place during the short time that the machine is hooked up to you.

    Ambulatory  ECG  methods  enable  your  doctor  to  study  longer periods of the heart’s activity while you go about your normal routine. Ambulatory  ECGs  are available in the form of a Holter monitor , which you wear for 24 to 48 hours  and which provides a continuous readout.  Your doctor  compares the ECG  recordings  with your account  of your activities and symptoms to see if an arrhythmia is occurring,  how often it occurs, and how it relates to the daily log of your activities. Also, the effectiveness of any antiarrhythmic medica- tions you may be taking can be monitored. However,  if your arrhyth- mia  is very infrequent, 48  hours  of Holter monitoring may  not capture  it.

    An event monitor   is another  ambulatory  ECG,  one that allows for longer  recording—as  long as 30 days. You activate the device yourself if you sense symptoms. The monitor’s recording system is “looped” to continuously  record and erase, so that when you activate it, it can retrieve data from 1 to 4 minutes prior to that time.

    Your doctor may want to order exercise stress testing  to see if an arrhythmia is brought  on by exercise. If you have had faint- ing spells, you may be asked to have a tilt-table  study  to observe how your heart responds to a change in position. This informa- tion  helps  your  doctor  determine how to  prevent  fainting  episodes. Echocardiography  may also be used to determine if there is structural  heart disease that may be causing arrhythmias.

    Electrophysiologic studies  are done in a hospital setting to more speci?cally study an arrhythmia,  test the effect of medications, and perform  some treatments  such as catheter  ablation. Electrophysio- logic studies are generally done by threading catheters through  the veins into  your heart  in order  to record  electrical signals and stimulate  the heart to induce an arrhythmia, to provide more precise information about your heart rhythms. Because the test requires that catheters are placed in your veins, it is described  as an invasive study. However,  with proper preparation,  electrophysiology studies can be performed with little or no discomfort  and are among the safest of all invasive tests. Also, impor- tantly, if possible, some arrhythmias are treated or cured at the same sit- ting during your electrophysiologic studies, with only a small risk to you.

    Electrophysiology studies  require  taking  periodic  X-rays via ?uo- roscopy during the procedure to determine where the catheter is within the heart. In some cases, transesophageal echocardiography may be used.

    Substances That Can Affect Heart Rhythm

    Thousands of substances have the potential to affect the electrical signals that stimulate your heartbeat. The impact of any one of them on you can range from harmless to severe. If you are diagnosed with a heart arrhythmia, be aware of your own exposure to some of these substances, and talk to your doc- tor about how they might be affecting your symptoms, the effects of your med- ications, or your overall heart health.
    • Caffeine in coffee, soft drinks, tea, or chocolate
    • Alcohol
    • Tobacco, including secondhand smoke
    • Diet pills
    • Some over-the-counter cough and cold remedies (especially those with pseudoephedrine)
    • Some herbal remedies (such as ephedra or ephedrine)
    • Prescription drugs (such as antianxiety, antipsychotic, or antiarrhythmic medications)
    • Bronchodilators, whether prescription or over-the-counter
    • Automobile emissions
    • Industrial pollution
    • Paint thinners
    • Propane gas
    • Hazardous substances in the workplace (such as carbon monoxide)

  • Types of Arrhythmia

    Irregularities in your heart rhythms can be described by the effect they have on the speed of your heartbeat (acceleration or deceleration) and where they occur in your heart (in the atria or in the ventricles). Another type of arrhythmia, called heart block, is a partial or complete interruption in the transmission of the electrical impulses between the upper and lower chambers of your heart.

    Bradycardia and Tachycardia

    An irregular heartbeat can be either too slow (bradycardia) or too fast (tachycardia). A healthy person generally has a resting heart rate of 60 to 100 beats per minute.
    Bradycardia, a heart rate of less than 60 beats per minute, may not be a medical problem. A physically active person whose heart pumps very ef?ciently may have a lower heart rate that is not at all abnormal. But a very slow heart rate can become a problem if the brain does not receive enough blood, causing symptoms such as light-headedness or fainting.
    Bradycardia most commonly affects older people because with age- related damage of the heart’s electrical system, all the impulses from the atrium may not get to the ventricle. It may be caused by damage to the sinoatrial node (where the electrical pulse begins) or to the biological “wires” that connect the upper chambers (atria) to the lower chambers (ventricles). This damage may be brought on by heart disease, aging, a genetic defect, or some drugs or medications. Medications or a tempo- rary pacemaker can speed up the heart’s contractions temporarily. A pacemaker is also a long-term treatment.
    Tachycardia, a very rapid heart rate of more

    than 100 beats per minute, can take many forms, depending on where in the heart it occurs. Fibrillation, perhaps the most serious form of tachycardia, causes the heart muscle to quiver instead of contracting rhythmically. (For symptoms, see page 258.) The heartbeat is not only too fast but uncoordinated as well. Both tachycardia and ?brillation, in various forms, can be treated with medications, surgery, or mechanical devices.

    Heart Block

    Heart   block  is a  condition in  which  the sinoatrial  node  sends  a normal  electrical impulse,   but  the  signal  does  not   travel through the  atrioventricular node  and into the ventricles  as it should. Therefore, there may be inef?cient  contraction of the ventri- cles. It usually occurs as a result of aging, or because  the  heart  is scarred  from  chronic heart disease such as coronary  artery disease or from valvular heart  disease (which a per- son may be born  with). Prior  heart  surgery may also cause scarring. Certain  medications that  slow the  electrical  conduction through the  heart—for  example, digitalis, beta-blockers, or some calcium blockers—can  worsen heart block.

    Heart  block is classi?ed into three groups, according to how severe it is. In ?rst-degree heart block, the electrical impulse moves too slowly through the  atrioventricular node.  Your doctor  may refer  to the  PR interval,  which  is a part  of an  ECG  recording that  measures  the amount  of time it takes for an impulse to get from the atria into the ventricles (see page 265). If your PR interval is longer than 0.2 seconds, you have ?rst-degree heart  block. If your heart  rate and rhythm  are normal,  there  may be nothing wrong  with your heart.  In fact, some highly conditioned athletes also have ?rst-degree heart block. Usually, you will not require treatment for a ?rst-degree heart block. If you are taking medications  such as digitalis  or beta-blockers , the drug may be causing the condition.

    If you have second-degree heart  block,  some  signals from  your sinoatrial  node  do  not  reach  your  ventricles.  In  most  people  with second-degree block, impulses  are progressively  delayed  in the  atri- oventricular  node with each heartbeat  until a full beat is skipped. This is called a Mobitz  type of block. You may have no symptoms,  or you may experience some dizziness, but the condition  is not serious. On an ECG,  the skipped beat will show up as a P wave that is not followed by a QRS wave—a tracing of a contraction in the atria that did not activate the ventricles (see page 265). In a Mobitz type II heart block, the inter- val between the P wave and the QRS wave remains constant,  but the atrioventricular node  intermittently blocks the  electrical  impulses.  A Mobitz type I block may pass on its own, but a Mobitz type II block is generally more serious and requires that you have a pacemaker implanted .

    In a person who develops third-degree or complete  heart block, no signals at all are passing from the atria into the ventricles. To compen- sate, the ventricles use their own secondary pacemaker to contract  and keep blood moving. But the heartbeats  generated  this way are slow and cannot  maintain  full heart  function.  On  an ECG,  the  relationship between  the  P wave and the  QRS  wave is completely  abnormal  (see page 266). A person with third-degree heart block may lose conscious- ness, may develop  heart  failure,  and  is at risk of cardiac  arrest.  A mechanical pacemaker must be implanted  on an emergency  basis. If it is not possible to put one in right away, a temporary  pacemaker device can be used to keep the person alive until surgery can be done.

    For all types of heart  block, the decision  of whether  to implant  a pacemaker  is based on the severity of the bradycardia  symptoms.  In some  cases, the  deciding  factor  is how  slow your  heart  rate  has become.

    Ventricular Arrhythmias

    Generally,  an arrhythmia in the ventricles is a more serious condition than one in the atria, because the ventricles perform  the heart’s essen- tial pumping  functions.  Most serious ventricular  arrhythmias occur in association with other forms of heart disease, rather than as an isolated problem.  A healthy  person  may have numerous isolated  extra heart- beats originating in the ventricle, and a person with normal heart func- tion  usually does  not  require  treatment. Ventricular tachycardia  is made up of several of these irregular  heartbeats in a row.

    Premature Ventricular Contraction

    Premature ventricular contractions  occur when your ventricles contract too soon and interrupt the normal heartbeat. They may happen without warning,  and often  occur after you have consumed  caffeine or taken over-the-counter medications  that  contain  ephedra  or ephedrine.  By themselves, premature contractions  may be harmless and often do not require treatment. But if you have another  heart condition  such as car- diomyopathy or heart failure, premature ventricular contractions  can be a warning  of more  serious or prolonged  rhythm  disturbances  such as ventricular tachycardia or ventricular ?brillation.

    Ventricular Tachycardia

    In a person with ventricular tachycardia, a series of ventricular contrac- tions  originates  from  a spot  within  the  ventricles,  and the  heartbeat quickens—from 100 to 250 beats per minute. The  initial concern with this form of tachycardia is that the arrhythmia  may interfere  with the ability to pump blood, and the person may become dizzy or faint. But ventricular tachycardia may deteriorate  without warning into ventricu- lar ?brillation, which is life-threatening.

    Therefore, ventricular  tachycardia  is considered  a medical  emer- gency. The  goal of treatment is to stop the rapid heartbeat,  with elec- trical  shock (de?brillation)  if necessary, and then  to prevent  it from recurring. If the heart cannot return to a normal rhythm, it may go into ventricular ?brillation,  which can be fatal in minutes.

    Ventricular Fibrillation

    Ventricular fibrillation  is the  most  dangerous  form  of arrhythmia, requiring  immediate  emergency  attention. In  this  form  of extreme tachycardia, several impulses may be ?ring from different locations in the heart, and the heart contractions are in chaos. Although the heart rate may be as high as 300 beats per minute,  the heartbeats are com- pletely  ineffective  and  very little  blood  leaves the  heart.  Since  the brain is the organ most sensitive to the loss of oxygenated blood, ven- tricular  ?brillation  causes unconsciousness.  Someone  should call 911 or  emergency  medical  services immediately  and  begin  cardiopul- monary  resuscitation (CPR)  immediately  if you  are  not  breathing properly.  Electric  shock (de?brillation)  is usually essential to restore heart rhythm,  to prevent severe damage to the brain and other organs. Cardioversion (see page  271) may be used  to  deliver  the  necessary shocks. As many as 250,000 people die suddenly each year from ven- tricular  ?brillation.

    A de?brillator (sometimes called an automated external de?brilla- tor, or AED) is an electronic device that emergency medical services personnel or other  trained “?rst responders” use to deliver shock to someone  whose   heart   is  fibrillating.  These  defibrillators  are now available in many public places such as health  clubs and airports.

    Supraventricular Arrhythmias

    An arrhythmia that  occurs  in either  of the  two  atria  of your  heart, located above your ventricles, is considered a supraventricular (or atrial) arrhythmia.

    Supraventricular Tachycardia

    Supraventricular (or atrial) tachycardia is a regular but very rapid heart- beat (more than 100 beats per minute) involving the upper chambers of the heart. It can occur in several different  forms, when regions of the atria other than the sinoatrial node (the natural pacemaker) develop the ability to ?re electrical impulses repetitively. The path that these “extra” impulses take determines  what type of tachycardia you have.

    In one type (atrioventricular nodal reentrant tachycardia), electrical impulses travel in an abnormal  circular path around  the atrioventricu- lar node between the atria and the ventricles, causing the heart to beat with  each  circle.  Another  form,  called Wolff-Parkinson-White syn- drome,  occurs when there  is an extra electrical  pathway between  the atria and ventricles that causes electrical impulses to arrive at the ven- tricles too soon, resulting in a rapid heart rate. Some are caused by short circuits or extra electrically active tissue in the heart. It turns out that these “reentry circuits” are the most common mechanism.

    If you have supraventricular tachycardia, you may experience palpi- tations  or  a sense that  the  heart  is ?uttering  or  racing.  Often  these symptoms  occur  abruptly  with  little  or  no  warning.  Some  people have shortness  of breath,  chest pressure  or pain, or light-headedness. These sensations may last for a few seconds or several hours. The symp- toms can be alarming,  but usually supraventricular tachycardia  is not life-threatening. Of course, if you have these symptoms, you should have your doctor  diag- nose and treat your condition.  Treatment with drugs (see page 268) can relieve symptoms, or a cardiac ablation procedure  (see page 269) can cure the condition.

    If you have severe symptoms and go to the emergency  room,  doctors  may give medica- tions that can stop the supraventricular tachy- cardia and thus relieve your symptoms rapidly. Also, if the  type of tachycardia  you have has not  yet been  diagnosed,  an ECG  performed while you are  experiencing  the  symptoms  is very helpful in determining the best long-term treatment.

    Atrial Fibrillation

    Atrial fibrillation  (AF) is the  most  common type of arrhythmia in the United States, occurring in 5 to 10 percent  of all people over 65. People over the age of 80 are especially vulnerable, too, although it can occur in some people who are 40 or younger. In a person with AF, the electrical impulse from the sinoatrial  node accelerates as it spreads across the atria, causing these upper chambers of the heart to quiver, contracting rapidly and irregu- larly—at rates of 400 to 600 beats per minute.  A specialized structure between the atria and the ventricles, the atrioventricular node, acts as a safeguard,  stopping  one or two of every three  signals from  the  atria before they reach the ventricles. But the ventricles still beat too rapidly and irregularly.

    AF may occur without  any associated heart  disease. However,  it is commonly  linked with hypertension (high blood  pressure),  coronary artery  disease, mitral  valve disease, pericardial  disease, lung  disease, cardiomyopathy, or thyroid disease. When AF occurs, it is important to slow the ventricular rate and then look for the cause and treat that.

    Several different  forms  of AF can occur,  and  the  symptoms  can vary widely. Some people experience AF only occasionally, with symptoms  such as palpitations  that  last from  a few seconds to a few days before  subsiding  spontaneously;  this form  is called paroxysmal atrial ?brillation.  In  a person  with  persistent  AF, episodes  do not  stop  by themselves, and drugs or other treatments—such as ablation or cardioversion  are required  to restore  normal heart rhythm. Permanent AF is constant and does not respond to treatment.  In these situations  treatment focuses on heart  rate control  and prevention  of blood clots. AF can cause symptoms of fatigue or short- ness of breath  and lead to ?uid buildup. Over time the heart rate may slow to the point of causing bradycardia .

    For  many people,  the  experience  of AF is unpleasant—causing  a sensation of palpitation  and unwellness—but  not necessarily harmful. Treatment can relieve the symptoms,  and AF is generally unlikely to advance  to  a more  serious  condition. But  having  palpitations  can be frightening and worrisome.  If you experience  palpitations  for the ?rst  time,  you should  always get medical  attention to  diagnose  the problem.

    AF can cause blood to pool in the atria, which can lead to blood clots. If a clot travels from the heart into a smaller artery in the brain, it can cause a stroke. About 15 percent of strokes occur in people with AF, and among  those with AF, the rate of strokes is about 5 percent  per year. Once  AF is diagnosed,  your  doctor  may prescribe  warfarin,  a blood thinner,  which prevents blood clots from forming and reduces the risk of stroke by two thirds. Risk factors for blood clots associated with AF include  advanced  age, diabetes,  high  blood  pressure,  previous  heart damage, and a history of stroke.

    Left untreated, AF can cause a chronic increase in heart rate, which can weaken the ventricles over time and cause heart failure. But most people seek treatment before this occurs.

    Atrial Flutter

    Atrial ?utter is another  common form of arrhythmia in which the atria beats rapidly but relatively regularly. It usually occurs when electrical impulses  are trapped  in an endless loop, typically in the  lower right atrium.  Although the atria may be contracting as quickly as 300 times per minute, the atrioventricular node allows only some of those beats to pass into the ventricles. Still, the ventricles are contracting too quickly and the heart is not pumping  as ef?ciently as it needs to. Atrial ?utter or atrial ?brillation  often occurs as a consequence  of a heart attack or surgery on the heart or lungs.

  • Interpretation of Acid-Base Data

    Acid-base data interpretation has always been one of the more difficult areas of laboratory medicine. In most uncomplicated untreated cases the diagnosis can be achieved with reasonable ease. There are several ways of approaching an acid-base problem. One way is to examine first the arterial PCO2 value. Since primary respiratory disorders result from hypoventilation or hyperventilation, which, in turn, are reflected by a change in arterial PCO2, normal PCO2 with abnormal pH is strong evidence against a primary respiratory disorder and should be an uncompensated metabolic disorder.

    If PCO2 is decreased, there are two major possibilities:

    1. The primary disorder could be respiratory alkalosis (hyperventilation). If so, pH should be increased in acute (uncompensated) cases or partially compensated cases. In fully compensated cases pH is within reference range, but frequently it is more than 7.40 even within the reference range.

    2. The primary disorder could be metabolic acidosis. If so, pH should be decreased in partially compensated cases. In fully compensated cases pH is within its reference range (similar to fully compensated respiratory alkalosis), but frequently it is less than 7.40 even within the reference range.

    If PCO2 is increased, there are also two major possibilities:

    1. The primary disorder could be respiratory acidosis (hypoventilation). If so, pH should be decreased in acute (uncompensated) cases or partially compensated cases. In fully compensated cases pH is within reference range, but frequently it is less than 7.40 even within reference range.

    2. The primary disorder could be metabolic alkalosis. If so, pH should be increased in partially compensated cases. In fully compensated cases pH is within its reference range (similar to fully compensated respiratory acidosis), but pH frequently is more than 7.40 even within the reference range.

    There is another way to interpret the data. If one first inspects pH, decreased pH means acidosis and increased pH means alkalosis. One then inspects the PCO2 value. If the PCO2 has changed in the same direction as the pH, the primary disorder is metabolic. If the PCO2 has changed in the opposite direction from that of the pH, the primary disorder is respiratory.

    Base excess analysis is not a vital part of this type of algorithm. However, base excess can sometimes be helpful, both as additional evidence for certain types of acid-base disorders or to help detect the presence of active acid-base disorder in fully compensated cases. A negative base excess is found in metabolic acidosis and, to a lesser extent, in respiratory alkalosis. A positive base excess is found in metabolic alkalosis and, to a lesser extent, in respiratory acidosis.

  • Buffer Base and Base Excess

    The concepts of buffer base and base excess form part of the Astrup acid-base system. The term buffer base refers to all substances in the buffering system of whole blood that are able to bind excess H+. Bicarbonate forms slightly more than one half of the total buffer base; hemoglobin makes up about one third of the total buffer base, consisting of three fourths of the nonbicarbonate buffer system. Normal buffer base values for any patient are therefore calculated on the basis of the actual hemoglobin concentration as well as normal values for pH and HCO–3. The term base excess refers to any difference in the measured total quantity of blood buffer base from the patient’s calculated normal value. Thus, an increase in total buffer base (e.g., an increase in HCO–3) is considered a positive base excess; a decrease in total buffer base from calculated normal (e.g., a decrease in HCO–3) is considered a negative base excess (some prefer to use the terms “base excess” and “base deficit” rather than positive or negative base excess). Venous blood has a base excess value about 2.0-2.5 mEq/L higher than arterial blood.

  • Arrhythmias

    Every second or so, an electrical impulse originating in the right atrium of your heart travels through the heart and triggers a single heartbeat, or contraction of the heart. A group of specialized cells in the muscle tissue, called the sinoatrial (SA) node, initiates the signal, acting as your heart’s natural pacemaker. The impulse travels through the four chambers of your heart in a carefully timed sequence to stimulate the rhythmic contractions that pump blood through your body (see pages
    9–10).
    Any change or interruption in the electrical signal that throws off this rhythm is called an arrhythmia. The heart may beat too fast, too slow, or in an irregular pattern. Arrhythmias can occur in people with normal hearts or those with underlying disease. Throughout the course of your lifetime, your heart will occasionally skip a beat or palpitate slightly, and these brief variations are completely harmless. Some people have minor arrhythmias that never cause a problem. However, in some arrhythmias, the pumping action of the heart can be seriously affected, or it can cause symptoms of palpitation (awareness of the abnormal heartbeat), light-headedness, or fainting. If you have another heart condition, such as heart failure, an arrhythmia is more likely to cause a problem for you.
    Some people are born with an irregular heartbeat. Other cardiovascular conditions, such as high blood pressure, valvular disease, heart failure, or coronary artery disease can be factors; diabetes can also con- tribute (see page 105). Substances such as caffeine, tobacco, alcohol, cocaine and prescribed medication, some over-the-counter cough and cold medications, diet pills, and some herbal remedies can affect the pattern of your heartbeat (see page 267). Stress can also cause arrhythmias in some people, as the body releases adrenaline, the stress hormone. Low levels of or an imbalance of electrolytes such as low potassium levels may cause or worsen an arrhythmia. Your doctor may order a blood test to check your electrolytes, to make sure there is no correctable problem causing your arrhythmia.
    Treatment, therefore, may include lifestyle changes and control of other conditions, taking an antiarrhythmia medication, avoiding some medications, nonsurgical procedures, or surgery (for instance, implantation of a pacemaker) to restore a normal heartbeat. Your doctor may refer you to a heart rhythm specialist, called an electrophysiologist.

  • Acid-Base Compensation

    Compensation refers to the degree of PCO2 change when there is, or has been, an abnormality in pH.

    An uncompensated disorder is a primary metabolic or respiratory condition that has not been altered by any significant degree of correction. In the case of a primary metabolic condition the respiratory counterbalance (change in ventilation which is reflected by a change in arterial PCO2) is not evident; pH is abnormal but PCO2 remains normal. In the case of a primary respiratory condition, both PCO2 and pH are abnormal, and the degree of abnormality on both tests is relatively severe. In that case the renal counterbalance (increased bicarbonate formation to bring pH back toward normal) is not evident.

    A partially compensated disorder is present when both pH and PCO2 are outside their reference ranges. In primary respiratory disorders, the degree of pH abnormality is not as severe as in uncompensated cases.

    A fully compensated (sometimes referred to only as compensated) condition is a primary metabolic or respiratory disorder in which PCO2 is outside its reference range but pH has returned to its reference range.