Certain adrenal cortex hormones control sodium retention and potassium excretion. Aldosterone is the most powerful of these hormones, but cortisone and hydrocortisone also have some effect. In primary Addison’s disease there are variable degrees of adrenal cortex destruction. This results in deficiency of both aldosterone and cortisol, thereby severely decreasing normal salt-retaining hormone influence on the kidney. Sometimes there is just enough hormone to maintain sodium balance at a low normal level. However, when placed under sufficient stress of any type, the remaining adrenal cortex cells cannot provide a normal hormone response and therefore cannot prevent a critical degree of sodium deficiency from developing. The crisis of Addison’s disease is the result of overwhelming fluid and salt loss from the kidneys and responds to adequate replacement. Serum sodium and chloride levels are low, the serum potassium level is usually high normal or elevated, and the patient is markedly dehydrated. The carbon dioxide (CO2) content may be normal or may be slightly decreased due to the mild acidosis that accompanies severe dehydration. In secondary Addison’s disease, due to pituitary insufficiency, glucocorticoid hormone production is decreased or absent but aldosterone production is maintained. However, hyponatremia sometimes develops due to an increase in AVP (ADH) production by the hypothalamus. In primary aldosteronism there is oversecretion of aldosterone, which leads to sodium retention and potassium loss. However, sodium retention is usually not sufficient to produce edema, and the serum sodium value remains within the reference range in more than 95% of cases. The serum potassium value is decreased in about 80% of cases (literature range, 34%-92%). In Cushing’s syndrome there is overproduction of hydrocortisone (cortisol), which leads to spontaneous mild hypokalemia and hypochloremic alkalosis in 10%-20% of patients (usually those with more severe degrees of cortisol excess). Use of diuretics will induce hypokalemia in other patients. The serum sodium level usually remains within reference range.
Month: October 2009
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Hyponatremic Depletional Syndromes
In protracted and severe vomiting, as occurs with pyloric obstruction or stenosis, gastric fluid is lost in large amounts and a hypochloremic (acid-losing) alkalosis develops. Gastric contents have a relatively low sodium content and water loss relatively exceeds electrolyte loss. Despite relatively low electrolyte content, significant quantities of electrolytes are lost with the fluid, leading to some depletion of total body sodium. The dehydration from fluid loss is partially counteracted by increased secretion of arginine vasopressin (AVP, or vasopressin; antidiuretic hormone, ADH) in response to decreased fluid volume. AVP promotes fluid retention. Whether hyponatremia, normal-range serum sodium values, or hypernatremia will develop depends on how much fluid and sodium are lost and the relative composition and quantity of replacement water and sodium, if any. Oral or parenteral therapy with sodium-free fluid tends to encourage hyponatremia. On the other hand, failure to supply fluid replacement may produce severe dehydration and even hypernatremia. Serum potassium values are most often low due to direct loss and to alkalosis that develops when so much hydrochloric acid is lost. Similar findings are produced by continuous gastric tube suction if continued over 24 hours.
In severe or long-standing diarrhea, the most common acid-base abnormality is a base-losing acidosis. Fluid loss predominates quantitatively over loss of sodium, chloride, and potassium despite considerable depletion of total body stores of these electrolytes, especially of potassium. Similar to what occurs with vomiting, decrease in fluid volume by fluid loss is partially counteracted by increased secretion of AVP (ADH). Again, whether serum sodium becomes decreased, normal, or increased depends on degree of fluid and electrolyte loss and the amount and composition of replacement fluid (if any). Sufficient electrolyte-free fluids may cause hyponatremia. Little or no fluid replacement would tend toward dehydration, which, if severe, could even produce hypernatremia. The diarrhea seen in sprue differs somewhat from the electrolyte pattern of diarrhea from other causes in that hypokalemia is a somewhat more frequent finding.
In extensive sweating, especially in a patient with fever, large amounts of water are lost. Although sweat consists mostly of water, there is a small but significant sodium chloride content. Enough sodium and chloride loss occurs to produce total body deficits, sometimes of surprising degree. The same comments previously made regarding gastrointestinal (GI) content loss apply here also.
In extensive burns, plasma and extracellular fluid (ECF) leak into the damaged area in large quantities. If the affected area is extensive, hemoconcentration becomes noticeable and enough plasma may be withdrawn from the circulating blood volume to bring the patient close to or into shock. Plasma electrolytes accompany this fluid loss from the circulation. The fluid loss stimulates AVP (ADH) secretion. The serum sodium level may be normal or decreased, as discussed earlier. If the patient is supported over the initial reaction period, fluid will begin to return to the circulation after about 48 hours. Therefore, after this time, fluid and electrolyte replacement should be decreased, so as not to overload the circulation. Silver nitrate treatment for extensive burns may itself cause clinically significant hyponatremia (due to electrolyte diffusion into the hypotonic silver nitrate solution).
Diabetic acidosis and its treatment provide very interesting electrolyte problems. Lack of insulin causes metabolism of protein and fat to provide energy that normally is available from carbohydrates. Ketone bodies and other metabolic acids accumulate; the blood glucose level is also elevated, and both glucose and ketones are excreted in the urine. Glucosuria produces an osmotic diuresis; a certain amount of serum sodium is lost with the glucose and water, and other sodium ions accompany the strongly acid ketone anions. The effects of osmotic diuresis, as well as of the accompanying electrolyte loss, are manifested by severe dehydration. Nevertheless, the serum sodium and chloride levels are often low in untreated diabetic acidosis, although (because of water loss) less often they may be within normal range. In contrast, the serum potassium level is usually normal. Even with normal serum levels, considerable total body deficits exist for all of these electrolytes. The treatment for severe diabetic acidosis is insulin and large amounts of IV fluids. Hyponatremia may develop if sufficient sodium and chloride are not given with the fluid to replace the electrolyte deficits. After insulin administration, potassium ions tend to move into body cells as they are no longer needed to combine with ketone acid anions. Also, potassium is apparently taken into liver cells when glycogen is formed from plasma glucose under the influence of insulin. In most patients, the serum potassium level falls to nearly one half the admission value after 3-4 hours of fluid and insulin therapy (if urine output is adequate) due to continued urinary potassium loss, shifts into body cells, and rehydration. After this time, potassium supplements should be added to the other treatment.
Role of the kidney in electrolyte physiology
In many common or well-recognized syndromes involving electrolytes, abnormality is closely tied to the role of the kidney in water and electrolyte physiology. A brief discussion of this subject may be helpful in understanding the clinical conditions discussed later.
Urine formation begins with the glomerular filtrate, which is similar to plasma except that plasma proteins are too large to pass the glomerular capillary membrane. In the proximal convoluted tubules, about 85% of filtered sodium is actively reabsorbed by the tubule cells. The exchange mechanism is thought to be located at the tubule cell border along the side opposite the tubule lumen; thus, sodium is actively pumped out of the tubule cell into the renal interstitial fluid. Sodium from the urine passively diffuses into the tubule cell to replace that which is pumped out. Chloride and water passively accompany sodium from the urine into the cell and thence into the interstitial fluid. Most of the filtered potassium is also reabsorbed, probably by passive diffusion. At this time, some hydrogen ions are actively secreted by tubule cells into the urine but not to the extent that occurs farther down the nephron (electrolyte pathways and mechanisms are substantially less well known for the proximal tubules than for the distal tubules).
In the ascending (thick) loop of Henle, sodium is still actively reabsorbed, except that the tubule cells are now impermeable to water. Therefore, since water cannot accompany reabsorbed sodium and remains behind in the urine, the urine at this point becomes relatively hypotonic (the excess of water over what would have been present had water reabsorption continued is sometimes called “free water” and from a purely theoretical point of view is sometimes spoken of as though it were a separate entity, almost free from sodium and other ions).
In the distal convoluted tubules, three processes go on. First, sodium ions continue to be actively reabsorbed. (In addition to the sodium pump located at the interstitial side of the cell, which is pushing sodium out into the interstitial fluid, another transport mechanism on the tubule lumen border now begins actively to extract sodium from the urine into the tubule cells.) Intracellular hydrogen and potassium ions are actively excreted by the tubule cells into the urine in exchange for urinary sodium. There is competition between hydrogen and potassium for the same exchange pathway. However, since hydrogen ions are normally present in much greater quantities than potassium, most of the ions excreted into the urine are hydrogen. Second, the urinary acidification mechanisms other than bicarbonate reabsorption (NaHPO4 and NH4) operate here. Third, distal tubule cells are able to reabsorb water in a selective fashion. Permeability of the distal tubule cell to water is altered by a mechanism under the influence of AVP (ADH). There is a limit to the possible quantity of water reabsorbed, because reabsorption is passive; AVP (ADH) simply acts on cell membrane permeability, controlling the ease of diffusion. Therefore, only free water is actually reabsorbed.
In the collecting tubules, the tubular membrane is likewise under the control of AVP (ADH). Therefore, any free water not reabsorbed in the distal convoluted tubules plus water that constitutes actual urine theoretically could be passively reabsorbed here. However, three factors control the actual quantity reabsorbed: (1) the state of hydration of the tubule cells and renal medulla in general, which determines the osmotic gradient toward which any reabsorbed water must travel; (2) the total water reabsorption capacity of the collecting tubules, which is limited to about 5% of the normal glomerular filtrate; and (3) the amount of free water reabsorbed in the distal convoluted tubules, which helps determine the total amount of water reaching the collecting tubules.
Whether collecting tubule reabsorption capacity will be exceeded, and if so, to what degree, is naturally dependent on the total amount of water available. The amount of water reabsorbed compared to the degree of dilution (hypotonicity) of urine reaching the collecting tubules determines the degree of final urine concentration.
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Hyponatremia. Iatrogenic Sources of Hyponatremia
Diuretic therapy and administration of IV hypotonic fluids (dextrose in water or half-normal saline) form very important and frequent etiologies for hyponatremia, either as the sole agent or superimposed on some condition predisposing to hyponatremia. In several studies of patients with hyponatremia, diuretic use was considered to be the major contributing factor or sole etiology in about 30% of cases (range, 7.6%-46%). In two series of patients with severe hyponatremia (serum sodium <120 mEq/L), diuretics were implicated in 30%-73% of cases. Hyponatremia due to diuretics without any predisposing or contributing factors is limited mostly to patients over the age of 55 years. IV fluid administration is less often the sole cause for hyponatremia (although it occurs) but is a frequent contributing factor. In one study of postoperative hyponatremia, 94% of the patients were receiving hypotonic fluids. If renal water excretion is impaired, normal maintenance fluid quantities may lead to dilution, whereas excessive infusions may produce actual water intoxication or pulmonary edema. There may also be problems when excessive losses of fluid or various electrolytes occur for any reason and replacement therapy is attempted but either is not adequate or is excessive. The net result of any of the situations mentioned is a fluid disorder with or without an electrolyte problem that must be carefully and logically reasoned out, beginning from the primary deficit (the cause of which may still be active) and proceeding through subsequent events. Adequate records of fluid and electrolyte administration are valuable in solving the problem. In nonhospitalized persons a similar picture may be produced by dehydration with conscious or unconscious attempts at therapy by the patient or relatives. For example, marked sweating leads to thirst, but ingestion of large quantities of water alone dilutes body fluid sodium, already depleted, even further. A baby with diarrhea may be treated at home with water or sugar water; this replaces water but does not adequately replace electrolytes and so has the same dilutional effect as in the preceding example. On the other hand, the infant may be given boiled skimmed milk or soup, which are high-sodium preparations; the result may be hypernatremia if fluid intake is not adequate.
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Serum Sodium Abnormalities
The most frequent electrolyte abnormalities, both clinically and as reflected in abnormal laboratory values, involve sodium. This is true because sodium is the most important cation of the body, both from a quantitative standpoint and because of its influence in maintaining electric neutrality. The most common causes of low or high serum sodium values are enumerated in the box. Some of these conditions and the mechanisms involved require further explanation.
Technical problems in sodium measurement may affect results. For many years the primary assay technique for sodium and potassium was flame photometry. Since 1980, instrumentation has been changing to ion-selective electrodes (ISEs). ISEs generate sodium results that are about 2% higher than those obtained by flame photometry (in patient blood specimens this difference is equivalent to 2-3 mEq/L [2-3 mmol/L]). Potassium values are about the same with both techniques. Many, but not all, laboratories automatically adjust their ISE sodium results to make them correspond to flame photometer values. Sodium concentration can be decreased in blood by large amounts of glucose (which attracts intracellular fluid, creating a dilutional effect). Each 62 mg of glucose/100 ml (3.4 mmol/L) above the serum glucose upper reference limit results in a decrease in serum sodium concentration of 1.0 mEq/L. Large amounts of serum protein (usually in patients with myeloma) or lipids (triglyceride concentration >1,500 mg/100 ml [17 mmol/L]) can artifactually decrease the serum sodium level when sodium is measured by flame photometry (values obtained by the ISE method are not affected). One report suggests a formula whose result can be added to flame photometry values to correct for severe
Clinical Situations Frequently Associated With Serum Sodium Abnormalities
I. Hyponatremia
A. Sodium and water depletion (deficit hyponatremia)
1. Loss of gastrointestinal (GI) secretions with replacement of fluid but not electrolytes
a. Vomiting
b. Diarrhea
c. Tube drainage
2. Loss from skin with replacement of fluids but not electrolytes
a. Excessive sweating
b. Extensive burns
3. Loss from kidney
a. Diuretics
b. Chronic renal insufficiency (uremia) with acidosis
4. Metabolic loss
a. Starvation with acidosis
b. Diabetic acidosis
5. Endocrine loss
a. Addison’s disease
b. Sudden withdrawal of long-term steroid therapy
6. Iatrogenic loss from serous cavities
a. Paracentesis or thoracentesis
B. Excessive water (dilution hyponatremia)
1. Excessive water administration
2. Congestive heart failure
3. Cirrhosis
4. Nephrotic syndrome
5. Hypoalbuminemia (severe)
6. Acute renal failure with oliguria
C. Inappropriate antidiuretic hormone (IADH) syndrome
D. Intracellular loss (reset osmostat syndrome)
E. False hyponatremia (actually a dilutional effect)
1. Marked hypertriglyceridemia*
2. Marked hyperproteinemia*
3. Severe hyperglycemia
II. Hypernatremia
Dehydration is the most frequent overall clinical finding in hypernatremia.
1. Deficient water intake (either orally or intravenously)
2. Excess kidney water output (diabetes insipidus, osmotic diuresis)
3. Excess skin water output (excess sweating, loss from burns)
4. Excess gastrointestinal tract output (severe protracted vomiting or diarrhea without fluid therapy)
5. Accidental sodium overdose
6. High-protein tube feedings*Artifact in flame photometry, not in ISE.
hyperlipidemia (triglyceride >1,500 mg/100 ml): % that Na value should increase = 2.1 Ч [triglyceride (gm/100 ml) – 0.6]. There is an interesting and somewhat inexplicable variance in reference range values for sodium in the literature, especially for the upper end of the range. This makes it highly desirable for each laboratory to determine its own reference range. Another problem is a specimen drawn from the same arm that already has an intravenous (IV) line; this usually happens when the phlebotomist cannot find a vein in the opposite arm. However, this may lead to interference by the contents of the IV system.
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Effect of Physiologic Patient Variation on Blood Gas Interpretation
There is a surprising degree of fluctuation in blood gas values in normal persons and in stabilized sick persons. In one study of normal persons using arterialized capillary blood, changes of at least 10% in bicarbonate or total CO2, 15% in PCO2, and 170% in base excess were required to exceed normal day-to-day variation. In another study, this time using arterial samples from stabilized ICU patients, average fluctuations within patients without known cause were found of 3.0 mm Hg (range 1-8 mm Hg) for PCO2, 0.03 pH units (range 0.01-0.08 units) for pH, and 16 mm Hg (range 1-45 mm Hg) for PO2. There were sufficient variation in repeat samples drawn at 10 minutes and at about 1 hour that a change of about 10% at 10 minutes and of about 20% at 1 hour was necessary to be considered significant. This suggests caution in making decisions based on small changes in acid-base or PO2 values.
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Newborn and Neonatal Blood Gas Measurement
A number of studies have found that umbilical cord arterial pH is the best available indicator of fetal acidosis, which would suggest intrauterine fetal hypoxia. Arterial pH was found to be more accurate than arterial PCO2, PO2, cord venous pH, or Apgar score. Although there is some disagreement regarding cord arterial pH reference range, a pH of 0.15 appears to be the best cutoff point (I obtained the same value in a group of 122 consecutive newborns).
There is also data from several studies of heelstick (or other capillary site) puncture specimens for blood gas PO2, PCO2, or pH measurement versus arterial specimens. The studies generally found adequate correlations in healthy term infants, less correlation in premature newborns, and increasingly poor correlation of all parameters as severity of illness increased, especially in premature newborns. The conclusion was that capillary blood gas results must be interpreted with much caution in severely ill newborns or neonates.
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Surgical Treatments for Arrhythmias
In addition to drugs and nonsurgical procedures, several types of surgery can restore your heart’s rhythm. Implantation of a pacemaker can treat bradycardia (slow heartbeat); an internal cardioverter- de?brillator can correct more serious arrhythmias; or a procedure called maze surgery can be performed on some people with atrial ?brillation.
Pacemakers
A pacemaker is a battery-powered unit that regulates your heart’s rhythm. Most pacemakers are implanted in people whose sinoatrial node is firing too slowly as a result of age, heart disease, or heart medications; the pacemaker takes over for the sinoatrial node if it fails to start. In a person with heart block, the device replaces a blocked pathway. Today pacemakers not only “pace” your heart’s rhythm but also have a “demand” sensor that can speed up or slow down your heart rate in response to your activity level, just as your heart would naturally.
The device itself, which is about the size of a man’s watch, contains a battery and an electronic pulse generator, with either one or two leads that are threaded into your heart. The device is programmed to read whether your heart rate is within an acceptable range for you. If it is not, the pacemaker generates an electrical impulse to stimulate a heart beat at an appropriate rate. A single-chamber pacemaker has one lead that is positioned in one heart chamber, the right atrium or ventricle; a dual-chamber unit has two leads that are threaded into both the right atrium and the right ventricle. The pacemaker can remain in place for several years before the batteries require replacement.
For people with heart failure or with certain physical characteristics, a third lead may be placed in the back of the heart through a side vein. This is called biventricular pacing. While more complicated to perform than the usual insertion of a pacemaker, this procedure can make some people with heart failure feel much better by coordinating the heart’s contractions.
How a Pacemaker Is Implanted
To have a pacemaker implanted, you will need only a mild sedative and a local anesthetic in the area of your upper chest. First the doctor makes a small incision in the skin under the collarbone. The thin, coated leads are threaded through a blood vessel under your collarbone and positioned in your heart under X-ray. Then they connect the leads to the pacemaker unit and slip it under your skin, also just under your collarbone. You will notice only a small bump at the site. The proce- dure will be over in 1 to 2 hours, and complications are rare. Serious or life-threatening complications occur in less than 1 percent of cases. Infection of the pacemaker is rare but generally requires that the pace- maker be removed. Sometimes less serious complications can occur such as bleeding, collapse of a lung, or the pacemaker’s leads may need repositioning.
You will probably be able to return to your routine activities in a few days. Your doctor may tell you to avoid heavy lifting or vigorous move- ment of your arm on the side of the pacemaker.
Living with Your Pacemaker
You will need to have regular checkups. The checkups are more frequent until the pacemaker site heals com- pletely; then they occur about every 3 to 6 months, for monitoring. Your doctor will evaluate your pacemaker by moving an electronic programmer over the device. The programmer relays information about pacemaker function and the life of the battery, and it can also change the programming (pacing instructions) of the device if necessary. In addition to the of?ce checkups,
your doctor may also give you instructions for how to have some monthly evaluations done by telephone.
When the battery begins to wear down, your pace- maker will slow down somewhat, but it won’t stop sud- denly. Your doctor will be able to detect the first warnings that the battery is running down before you have any sensation of it. When the battery needs replacing, you will need surgery to implant a new device. This procedure requires local anesthetic, but because the leads usually do not need replacement, the procedure is somewhat simpler than the original implantation.
Your doctor will also give you an identification card that provides specific information about the device you have. It is important to show this card to health-care professionals and to airport security staff
Once your pacemaker is in place and the implant site has healed, you most likely can participate in all of your usual activities. You and your doctor can review any possible restrictions—such as full-contact sports— that might apply to you. Always feel free to ask your doctor about any questions you have about appliances, medical procedures, or other considerations that you
think might affect your pacemaker. In general, it’s a good idea to be aware of your surroundings and alert for any circumstances that might interfere with the electronic circuitry in your pacemaker.
Although your pacemaker is not likely to restrict your life in signif- icant ways, it is important to remember that there are many things your pacemaker cannot do. It cannot protect you, for instance, from a heart attack caused by blocked arteries. It also cannot necessarily replace your need for medications, including heart-related drugs for conditions such as high blood pressure, angina, or even other forms of arrhythmia.
Implantable Cardioverter-Defibrillators
The internal cardioverter-de?brillator (ICD) is a battery-operated unit, only slightly larger than a pacemaker, that is implanted under your skin to monitor and correct your heart’s rhythm. All current ICDs also func- tion as pacemakers. An ICD is usually placed in a person with a dam- aged heart (as from a heart attack) who has had or is at high risk of having life-threatening heart rhythms, such as ventricular tachycardia or ventricular ?brillation. It may also be used for some people with severe atrial ?brillation.
An ICD can deliver the same sort of low-energy, imperceptible pulses that a pacemaker does. Furthermore, the ICD monitors the heart using the same technology. De?brillators are different from pacemak- ers in that they also monitor for very fast heart rates as well as for bradycardia. The ICD can also deliver higher-energy pulses (shocks) to the heart when it detects more serious or sustained rapid arrhythmias. These stronger impulses are called de?brillation shocks, and they are often life-saving.
A person with an ICD can feel these stronger impulses—usually a single shock, but sometimes a series of them—and they are often described as feeling like a quick thump or kick in the chest. Depending on the level of consciousness you have at the time of the shock, it may be painful (if you are not sedated) or may not be painful (if you have received sedatives).
Like a pacemaker, an ICD has two parts: a pulse generator, including a battery and electronic circuitry, and a system of coated leads tipped with electrodes. Newer devices are as small as a pager. They are also designed to provide a controlled burst of impulses, called overdrive pacing, at the first sign of ventricular tachycardia. If that does not restore normal heart rhythms, the device delivers de?brillation shock.
The devices make decisions on what type of therapy to give based on how fast the heart rate is. The devices are also equipped to regulate bradycardia (slow heartbeat) if that occurs. They also have a memory to record arrhythmic episodes and do some internal electrophysiologic testing.
In a person who has experienced prolonged ventricular arrhythmia, the ICD is more effective than antiarrhythmic drugs at preventing sudden death. The device may also similarly prevent cardiac arrest in a person who is considered at high risk of developing such arrhythmias. Before you are considered as a candidate for an ICD, your doctor must rule out other causes of the arrhythmia, such as a heart attack, myocar- dial ischemia (inadequate blood ?ow to the heart; see page 161), or chemical imbalance and drug reactions, which can be treated in other ways.
How an ICD Is Implanted
The procedure for placing an ICD is very similar to that for a pacemaker (see page 273). At the hospital, you will be given a sedative and then a local anesthetic. The cardiologist or surgeon will make an incision in the skin and then tunnel the leads through blood vessels into your heart, or onto its surface. Then he or she will tuck the ICD into a pouch of skin under the collarbone or somewhere above the waistline. The leads will be attached to the pulse generator. Electrophysiologic testing will be done to check out the device. The entire procedure takes about 2 hours.
You will probably stay in the hospital overnight. You may be prescribed some antiarrhythmic medications, too. These drugs may lessen the need for high-energy shocks from your ICD. The recovery time, the pain after the procedure, and risks of the procedure are very similar to those of a pacemaker.
After Implantation
After your ICD is installed, you will need to return to the doctor’s of?ce for monitoring every 1 to 3 months. Your doctor can evaluate the ICD function electronically by moving a programming wand over your chest. By this means, he or she can determine what kinds of impulses have been delivered, whether they worked, whether they need modi?- cation, and how much energy is left in the battery. When the energy level in the battery is down to a predetermined level, you will be scheduled for replacement surgery. The battery usually lasts from 3 to 5 years, depending on how many shocks it delivers. Usually, replacement surgery is somewhat simpler than the original implantation because the leads do not need to be replaced. Some ICDs can also be checked periodically by telephone.
Many people feel some apprehension about the possibility of receiv- ing unexpected de?brillation shocks. You may need to continue to take antiarrhythmia medications to reduce the risk of needing a shock from the implanted device. Some shocks are small, and some people don’t notice them. When you do receive a stronger shock, it may feel like a jolt, thump, or blow to the chest. Some people black out during periods of ?brillation, so they don’t feel the shock; see “Living with an ICD,” next section, on driving if you have an implanted ICD. If someone is touching you during the shock, he or she may feel a tremor, but will not be harmed by it in any way.
You and your doctor can discuss what to do if your ICD delivers a shock. Your doctor may tell you to call him or her if you feel a shock, or if you feel ill after the shock.
Apart from the discomfort of a sudden de?brillation shock, possible side effects of ICD placement include some sensitivity at the site of the implant, especially in very slender people; very rare problems with infection; and some cosmetic issues (the device is visible under the skin). If you feel apprehension about the shocks or concern about your need for an ICD, ask your doctor about a support group, where you can talk with other ICD “users” and medical staff.
You will also be given an identi?cation card that provides speci?c information about your ICD. Carry it with you at all times, and show it to health-care professionals and airport security.
Living with an ICD
As with a pacemaker, your ICD can interact with some devices in your environment with electromagnetic or radiofrequency ?elds. Review the interactions with implantable devices (see page 276), and talk to your doctor in detail about how devices in your environment, medical proce- dures, or your activities might affect your ICD.
Driving is a major consideration for a person with an ICD. Your ICD may take an interval of 5 to 15 seconds or longer to detect arrhythmias and deliver treatments, during which you might feel dizzy or even faint. Therefore, you are usually advised to avoid driving, and other activities, such as piloting or scuba diving, that would put you and others at risk if you were to lose consciousness. In some states, these restrictions are law. Review this issue with your doctor carefully. Some people who go for long periods without shock or symptoms are allowed to return to driving, but only with the advice of a doctor.
Maze Surgery
In some people with chronic atrial ?brillation, an operation called the maze procedure involves making a series of incision lines within the heart to create a maze that blocks electrical pathways through the heart muscle. This surgery is done in a person for whom medications, a pace- maker, or other treatments have not been effective. A likely candidate might be a person with uncontrolled atrial ?brillation, for whom the chief danger is that blood will pool in the upper chambers of the heart (the atria); this pooling increases the tendency of the blood to clot, which could lead to a stroke. The surgery may be performed with cer- tain other types of heart surgery to prevent atrial ?brillation after the operation.
The procedure is major surgery, done with the patient under general anesthesia. The surgeon must split the breastbone to expose the heart and transfer the functions of the heart and lungs to a heart-lung machine during the procedure.
The surgeon makes a number of small incisions in both the left and right atria. These incisions form a pattern that will direct the heart’s electrical impulses into the ventricles and block extra impulses. As the incisions heal, scar tissue forms that cannot conduct electrical impulses,
so the new pathways are permanently established. The surgery takes about 3 hours. Sometimes a pacemaker is implanted, too.
Recovery from maze surgery requires about 1 week in the hospital. You may need diuretics to prevent ?uid accumulation, and antiplatelet medication such as aspirin to prevent blood clots. You may experience pain from the chest incision, and fatigue for 2 to 3 months after surgery. Most people can go back to normal activities, including work, in about 3 months.
The maze procedure has been adapted to a less invasive technique, similar to a catheter-based ablation technique for atrial ?brillation. The technique allows the radiofrequency to be directed to the outside of the heart. This technique is complementary to less-invasive catheter-based ways to perform ablation of atrial ?brillation through the veins.
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Noninvasive Measurement of PCO2, PO2, and Oxygen Saturation
There are now several ways to measure carbon dioxide and oxygen in blood without drawing a blood sample. The two most popular methods at present are transcutaneous electrode systems and pulse oximetry. Both systems can provide continuous readings.
The transcutaneous systems use PCO2 and PO2 electrodes similar to those of standard arterial blood gas analysis applied directly to the skin over a gel sealant. Skin has capillaries close to the surface, and the tissues are permeable to some extent for carbon dioxide and oxygen. The apparatus heats the skin to 44°C to produce arterialized blood, thereby dilating the capillaries and increasing oxygen loss. The electrode sensors detect the carbon dioxide and oxygen diffusing from the capillaries. The apparatus must be moved at least every 4-6 hours in adults and 2-4 hours in infants to prevent thermal burns. The apparatus must be calibrated with a standard arterial blood gas sample obtained by arterial puncture each time the apparatus is positioned due to variability from differences in fat content (which interferes with gas diffusion) and skin thickness. Patient edema, hypothermia, or poor tissue perfusion (shock or vasoconstriction) interfere to varying degrees with accurate measurements.
Pulse oximetry measures hemoglobin oxygen saturation (percentage of hemoglobin structurally capable of binding oxygen that is saturated with oxygen) rather than oxygen tension (PO2). The method uses two light beams, one red and the other infrared, which are passed through tissue that contains arterial blood. Opposite to the light emitters are light detectors. The light detectors perform two tasks. First, they recognize and analyze arterial blood exclusively by differentiating those areas that have pulsation, and therefore changes in light transmission, from nonvascular tissue and nonarterial vascular components. Then oxygen saturation is measured in the pulsating vessels using the fact that changes in oxygen content have a significant effect on absorption of red light. The amount of red light absorption (transmission) is compared to that of the infrared light, which is affected much less. This system does not have to be calibrated by arterial puncture blood and does not have to be moved frequently. The instrument is accurate between saturation levels of about 70%-100%. When PO2 is above 100 mm Hg, hemoglobin is usually 100% saturated, reaching the upper limit of the oximeter. Below 70% saturation, accuracy becomes less, but trends in saturation change can be recognized. Carboxyhemoglobin can interfere with measurement. Since the instrument measures only oxygenation, acid-base abnormalities must be detected or investigated by some other method.
Abnormal results from either transcutaneous monitors or pulse oximeters must be confirmed by arterial puncture blood gas measurement. The pulse oximeter is usually attached to a toe in infants, to a finger in adults, and to the nose in obese adults.
Noninvasive continuous oxygen monitors are especially useful during anesthesia since most serious problems involve episodes of hypoxia; in premature or sick neonates and infants; in patients on ventilators; and in intensive care unit (ICU) patients or other unstable seriously ill adults.
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Nonsurgical Treatments for Arrhythmias
Great advances have been made in nonsurgical treatments for certain types of arrhythmias. These techniques, including ablation and electrical cardioversion, may restore normal heart rhythms, reduce or elimi- nate symptoms, and reduce or eliminate the need for medications or surgical procedures (such as implantation of a pacemaker or an internal cardioverter-de?brillator).
Catheter Ablation
Catheter ablation is now widely used to treat many types of tachycardia (rapid heartbeat), including atrial ?brillation, atrial ?utter, and atrial tachycardia, as well as some ventricular tachycardias. To perform catheter ablation, a doctor specializing in the treatment of arrhythmias (an electrophysiologist) threads one or more electrode-tipped catheters into the heart chambers and uses some form of energy—usually radiofrequency—to destroy (ablate) abnormal tissue that is generating extra impulses. The area of tissue that is eliminated is very small (about one-?fth of an inch across) and is not signi?cant to overall heart func- tion. A small, harmless scar forms at the site, and normal heart rhythm resumes.
The procedure has a high success rate and a low risk of complications, and requires only mild sedation and local anesthetic. It causes little or no discomfort, and most people can return to their daily activities in a few days. Many people are cured of their tachycardia, so they no longer need to take antiarrhythmic medication.
How Ablation Is Done
If you have ablation done, your doctor will probably tell you to stop taking any antiarrhythmic medications for several days before the
procedure. At the hospital, you will be given a mild sedative and a local anesthetic. The doctor will make one or more small punctures in your groin and in one side of your neck, your elbow, or just under your collarbone. He or she will thread catheters through your veins or arteries and into the heart. The procedure is done with X-ray guidance via ?uo- roscopy in real time, so the doctor can see the progress of the catheter.
Then the doctor often needs to start an episode of tachycardia in order to determine exactly where the arrhythmia is coming from. Using recordings of electrical activity from inside the heart, he or she “maps” the tissue to locate the problem area. Once the site is identi?ed and the ablation catheter is positioned, the radiofrequency energy is turned on and the abnormal tissue is destroyed. To ensure that all abnormal tissue has been eliminated, the doctor may test you with medications or elec- trical stimulation to see if the tachycardia can be induced again. If it can be, he or she repeats the ablation procedure. When the tachycardia can no longer be initiated, the catheters are removed. The entire procedure lasts from 2 to 4 hours.
You will stay in the hospital for at least a few hours, while doctors watch for recurring symptoms, rhythm disturbances, or bleeding from the catheterization sites. You may be able to go home after this obser- vation period, or you may need to stay overnight.
You can probably be moderately active, walking and climbing stairs, almost immediately. Many people go back to work or school in a few days. Your doctor may recommend that you take aspirin for 2 to 4 weeks to thin your blood so that clots do not form at the ablation sites in your heart. You will probably return for a follow-up visit to the electrophys- iologist in a few weeks.
Complications from ablation are rare but can be serious. Depending on the type of arrhythmia treated, and where in your heart the ablation is done, you could develop heart block (requiring a pacemaker) or expe- rience bleeding around the heart. However, the chance of heart attack, stroke, or death from ablation is quite rare.
In people with supraventricular arrhythmia and no other heart dis- ease, a complete cure of tachycardia is achieved by ablation more than
95 percent of the time. In people with ventricular arrhythmia, the cure rate is also high.
In people with other heart problems, such as a previous heart attack resulting in heart muscle damage or in heart muscle problems, an inter- nal defibrillator is almost always implanted as well (see page 275).
Rather than curing the tachycardia entirely, catheter ablation helps reduce the number of times the de?brillator is acti- vated. Sometimes to achieve a cure, though, more than one session of ablation is needed.
Cardioversion
Cardioversion is the medical term for restoration of your heart’s normal rhythm.
Cardioversion can be done either chemi-
cally (with drugs) or electrically (with shock). Atrial fibrillation, ventricular tachycardia, and ventricular ?brillation are the types of arrhythmia most commonly
treated with cardioversion. Ventricular ?brillation, the most serious type of arrhythmia, can only be treated with electrical shock.
If your doctor chooses to treat your atrial ?brillation with antiar- rhythmic drugs, he or she may give you the medications to take at home. But ?rst you take blood thinners for several weeks. Or the doc- tor may admit you to the hospital to give you the antiarrhythmia drugs either intravenously or by mouth, where hospital staff can check to see how you respond to treatment, and equipment can be used to monitor your heart rate and rhythm. Your symptoms, the medication your doc- tor is giving you, and the presence of other heart conditions (if any) will be factors in this decision.
If your doctor recommends electrical cardioversion (sometimes called direct-current or DC cardioversion), the procedure will be done in a hospital. It involves delivering a synchronized electrical current through paddles that touch your chest wall and allow the current to travel to your heart. The shock causes all of your heart cells to contract simultaneously, which stops the abnormal electrical signals without damage to the heart. Then the heart returns to a normal heartbeat.
How Electrical Cardioversion Is Done
Before you have a cardioversion done, your doctor will probably pre- scribe blood thinners such as warfarin for 3 to 4 weeks to reduce your
risk of blood clots. If you take other medications, you should take them as usual unless you are told otherwise. On the day of the procedure, do not eat after midnight. Also, do not use any skin lotions on your back and chest, because they could interfere with the cardioversion apparatus.
In the hospital, you will be given an intravenous sedative, possibly by an anesthesiologist. The doctor will place cardioversion pads (or paddles) on your chest and back, on either side of your heart. The pads are connected to an external de?brillator so that your heart rhythms can be monitored and regulated. Once you are asleep, the doctor will deliver the shock so that the current ?ows across your heart. If the ?rst shock does not restore your normal heart rhythm, the doctor can deliver gradually increased levels of current.
After the procedure, you will probably awaken quickly without any memory of the experience. You may have some minor chest discomfort or skin irritation where the pads were placed. You will probably be able to go home within an hour after the procedure. Have someone else drive you home, and do not drive or try to make any important deci- sions for the rest of the day, until the effects of the sedative are entirely gone. You will need to continue taking warfarin until your physician tells you to stop; periodic blood tests will check your clotting time.
Electrical cardioversion restores normal heart rhythms about 90 per- cent of the time. About half of the people who have the procedure relapse within a year; if so, the procedure can be repeated.
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Blood Lactate
Under conditions of adequate or near-adequate tissue oxygenation, glucose is metabolized for energy production using the aerobic metabolic pathway that converts glucose metabolic products to pyruvate that is, in turn, metabolized in the citric acid (Krebs) cycle. Under conditions of severe tissue hypoxia, aerobic metabolism cannot function properly, and glucose metabolic products at the pyruvate state stage are converted to lactate (lactic acid) by anaerobic metabolism. Therefore, increase in blood lactate is one indication of significantly decreased tissue oxygenation. Compared to other indicators of abnormal oxygen availability, PO2 decrease is best at suggesting decreased pulmonary alveolar uptake of oxygen, oxygen saturation methods demonstrate arterial oxygen content, and blood lactate shows the metabolic consequence of tissue hypoxia. In general, blood lactate is a fairly sensitive and reliable measurement of tissue hypoxia. It can be used to diagnose clinically important tissue hypoxia, to determine (roughly) the degree of hypoxia, to estimate tissue oxygen debt (the size of the accumulated oxygen deficit accumulated during a period of hypoxia), and to monitor the effect of therapy. Lactate can be increased in local ischemia if severe or extensive enough (e.g., grand mal seizures, or severe exercise; mesenteric artery insufficiency) as well as generalized ischemia (cardiac decompensation, shock, or carbon monoxide poisoning). The majority of patients exhibiting relatively large increases in blood lactate have metabolic acidosis, either primary or mixed (with respiratory acidosis or alkalosis).
Lactic acidosis has been divided into two groups: tissue hypoxia (discussed above) and conditions not involving significant tissue hypoxia. In the latter group are included severe liver disease (decreased metabolism of lactate), malignancy, drug-induced conditions (e.g., from cyanide, ethanol, and methanol), and certain inborn errors of metabolism. Idiopathic lactic acidosis associated with diabetes appears to combine a minor element of tissue hypoxia with some unknown triggering factor. In general, etiologies not primarily associated with tissue hypoxia tend to have lesser degrees of blood lactate elevation and better survival (with the exception of idiopathic lactic acidosis). However, there is a very significant degree of overlap in survival between the two classification groups. Another problem is controversy over definition of lactic acidosis. One frequently accepted definition is a lactate reference range of 0.5-1.5 mEq/L (mmol/L), hyperlactatemia when blood lactate persists in the 2.0-5.0 mEq/L range, and lactic acidosis when blood lactate exceeds 5 mEq/L (mmol/L) accompanied by metabolic acidosis. RBC metabolism increases lactate, so that specimens need special preservatives plus immediate ice cooling with early separation of the plasma, or else a bedside whole-blood analyzer.