Articles on Medical Diseases and Conditions

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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.

  • 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.

  • 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.

  • 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.

  • 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.

  • 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)