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  • 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.

  • Partial Pressure of Carbon Dioxide (PCO2) as a Measure of Respiratory Function

    In addition to its use in the Henderson-Hasselbalch equation, PCO2 provides information on pulmonary alveolar gas exchange (ventilation). If PCO2 is high, there is not a sufficient degree of alveolar ventilation. This may be due to primary lung disease (inability of the lungs to ventilate properly) or to some other reason. If PCO2 is low, there is alveolar hyperventilation, again either from primary or secondary etiology.

  • Summary of Acid-Base Changes

    To summarize plasma pH problems, in metabolic acidosis there is eventual HCO–3 deficit, leading to decreased plasma pH and decreased CO2 content (or CO2 combining power). In respiratory acidosis there is primary H2CO3 excess, which causes decreased plasma pH, but the CO2 content is increased due to renal attempts at compensation. In metabolic alkalosis there is eventual bicarbonate excess leading to increased plasma pH and increased CO2 content. In respiratory alkalosis there is primary carbonic acid deficit, which causes increased plasma pH, but the CO2 content is decreased due to renal attempts at compensation. The urine pH usually reflects the status of the plasma pH except in hypokalemic alkalosis, where there is acid urine pH despite plasma alkalosis.

    As noted, CO2 content or combining capacity essentially constitutes the numerator of the Henderson-Hasselbalch equation. PCO2 is essentially a measurement of the equation denominator and can be used in conjunction with pH to indicate acid-base changes. This is the system popularized by Astrup and Siggaard-Anderson. PCO2 follows the same direction as the CO2 content in classic acid-base syndromes. In metabolic acidosis, PCO2 is decreased, because acids other than H2CO3 accumulate, and CO2 is blown off by the lungs in attempts to decrease body fluid acidity. In metabolic alkalosis, PCO2 is increased if the lungs compensate by hypoventilation; in mild or acute cases, PCO2 may remain normal. In respiratory alkalosis, PCO2 is decreased because increased ventilation blows off more CO2. In respiratory acidosis, PCO2 is increased because of CO2 retention due to decreased ventilation.

  • Respiratory Alkalosis

    The other major subdivision of alkalosis is respiratory alkalosis, which occurs when the respiratory mechanism blows off more CO2 than it normally would due to respiratory center stimulation from some cause. The main conditions in which this happens are the hyperventilation syndrome caused by hysteria or anxiety, high fever, and direct stimulation of the respiratory center by drugs. Overdose of aspirin can cause respiratory alkalosis in the early stages; although later, after more of the aspirin is absorbed, a metabolic acidosis develops. In hyperventilation of whatever cause, respirations are increased and deeper, blowing off more CO2. This creates an H2CO3 deficit since it is being used up to replenish CO2 by the lung carbonic anhydrase enzymes. Therefore, the denominator of the Henderson-Hasselbalch equation is decreased, the 20:1 ratio is increased, and plasma pH increased. The CO2 content will decrease, because when H2CO3 is lost due to formation of CO2 in the lungs, HCO3– is converted to H2CO3 in the kidney to compensate secondarily for or to replace the decreasing plasma carbonic acid.

  • Metabolic Alkalosis

    Alkalosis may also be divided into metabolic and respiratory types. In metabolic alkalosis, three relatively common situations should be discussed.

    Alkali administration. Alkali administration most commonly occurs when sodium bicarbonate is taken in large quantities for the treatment of peptic ulcer symptoms. If this happens, excess HCO–3 is absorbed above the amount needed to neutralize stomach hydrochloric acid (HCl). The numerator of the Henderson-Hasselbalch equation is increased, the normal 20:1 ratio is increased, and the pH therefore rises. The CO2 content also rises because of the additional HCO–3. Lactate, citrate, or acetate in sufficient quantities may also produce alkalosis, since they are metabolized to HCO–3.

    Acid-losing alkalosis. Acid-losing alkalosis most frequently results from severe or protracted vomiting, as may occur with pyloric stenosis. Gastric HCl is lost in vomiting. Gastric HCl was originally produced by conversion of H2CO3 to HCO–3 and H+, mediated by carbonic anhydrase of the gastric mucosa. The HCO–3 is kept in the bloodstream, but the H+ is secreted into the gastric lumen as HCl. When HCl is lost through vomiting, the H+ component of HCl is also continually being lost. The CO2 content becomes increased, because the HCO–3 that is released when HCl is produced remains in the bloodstream and increases when additional HCl is formed to replace that which is being lost. Therefore, the 20:1 ratio is increased and the pH is increased. Since H2CO3 is decreased, as it is being continually used to produce more HCl, the lungs tend to retain CO2 to compensate. Therefore, PCO2 may actually increase, although not enough to prevent increase of the 20:1 ratio.

    Hypokalemic alkalosis. Hypokalemic alkalosis is most commonly due to excess potassium ion (K+) loss by the kidney, as might happen with overuse of certain diuretics that cause K+ as well as sodium ion (Na+) loss. Normally, most body K+ is intracellular, whereas most Na+ and H+ is extra-cellular. When excess K+ is lost in the urine, intracellular K+ diffuses out of the cells to replace some of that being lost from plasma; Na+ and H+ move into the cells to replace the K+ that has moved out. Thus, H+ is lost from extracellular fluid and plasma. A second mechanism depends on the fact that sodium is reabsorbed from the urine into the renal distal tubule cells by an active transport mechanism. This transport mechanism involves excretion of H+ and K+ into the urine to replace the reabsorbed Na+. In this exchange (or transport) system, H+ and K+ compete with each other. Therefore, if an intracellular deficit of K+ exists (in the tubule cells), more H+ is excreted into the urine to allow the reabsorption of the same quantity of sodium without losing as much K+. The result of renal H+ loss and extracellular H+ loss is an acid-losing type of alkalosis. Therefore, more H+ is manufactured by the kidney from H 2CO3 to replace lost extracellular fluid H+: more HCO–3 ions are thereby formed, and the numerator of the Henderson-Hasselbalch equation is increased. The denominator is eventually increased if the lungs attempt to compensate by increasing CO2 retention by slower breathing. However, respiratory compensation is frequently minimal or insignificant in hypokalemic alkalosis, so that the PCO2 frequently remains normal. Also, the urine pH is decreased because of the excess H+ being excreted in the urine. This is the opposite of what one would ordinarily expect, because in acidosis, the kidney usually attempts to compensate by excreting more H+(acid urine), whereas in alkalosis it normally tries to conserve H+ and thus produces a urine of higher pH (alkaline urine).

  • Respiratory Acidosis

    The second major category of acidosis is that called respiratory acidosis. This may be due to any condition that causes pulmonary CO2 retention. These conditions include the respiratory muscle paralysis of poliomyelitis, the respiratory brain center depression sometimes seen in encephalitis or with large doses of such drugs as morphine, primary lung disease (e.g., pulmonary fibrosis or severe emphysema) that destroys oxygen exchange ability, and sometimes heart diseases (e.g., chronic congestive heart failure). The basic problem is H2CO3 excess produced by CO2 retention. Thus, the denominator of the Henderson-Hasselbalch equation is increased, the normal 20:1 ratio is decreased, and the pH is decreased. The CO2 content is sometimes normal but is usually increased, because of kidney attempts to handle the excess CO2 by forming more HCO–3 and excreting more H+ ions.