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Experiments examining caffeine’s influence on pregnancy yield conflicting results buy cheap aciphex 10mg gastritis definicion, which may indicate the question is particularly complex or may simply mean that caffeine is an “invalid variable” having no effect buy aciphex 10 mg on line gastritis symptoms remedy. A 1994 survey of 259 women in the Netherlands found that caffeine raised the likelihood of becoming pregnant buy 20 mg aciphex free shipping gastritis kombucha, but when the same subject was examined in the 1980s among almost 2 buy aciphex 10 mg with mastercard lymphocytic gastritis diet,000 women in Connecticut, caf- feine was found to suppress fertility. During the 1990s a study of farm couples in Canada found that caffeine had no effect on fertility but that coffee-drinking women and tea-drinking men had lower birthrates, suggesting involvement of something besides caffeine in the natural products’ effect. Rat experimen- Caffeine 77 tation shows that caffeine reduces female fertility, produces smaller than usual offspring, and may affect brain development. Research in Yugoslavia indicates that pregnant women who do not smoke cigarettes but do take more than 71 mg of caffeine daily have smaller infants. A British study found the opposite; slightly smaller infants came from cigarette-smoking women who used 1,000 mg or more of caffeine a week, but the effect was not seen in nonsmokers. Still other studies find no connection between caffeine and either birthweight or prematurity. Caffeine affects vital signs in a human fetus even when the dose is so low as to have no influence on the pregnant woman. Question has arisen about whether caffeine promotes spontaneous abortion; a study published in 1994 found 140 mg to 280 mg a day to pose a significant risk; a rigorous study published in 1999 was unable to find such a hazard among moderate caffeine users; and a study published in 1993 saw caffeine as reducing the incidence of spontaneous abortion. Still another study found that women who drank decaffeinated coffee were even more likely to expe- rience a spontaneous abortion than women who drank caffeinated coffee. Testing caffeine on mice produced birth defects in limbs, and tests on chicken embryos produced heart deformities. Chicken embryos, however, are so sensitive to various chemicals that such results are not con- sidered a warning of human danger. Indeed, a substantial body of research indicates that caffeine causes no human birth defects. Evidence does exist that caffeine can increase the likelihood of birth defects caused by alcohol and tobacco. A statistical study showed that women who use more than 300 mg of caf- feine daily around the time of conception and who do not smoke are less likely to have infants with Down syndrome. Given all the uncertainties, pregnant women are advised to use caffeine “moderately”—no more than 200 mg to 300 mg daily (150 mg or less is con- sidered “minimal”). Caffeine increases milk production in nursing mothers and passes into the milk but appears unharmful to infants if the women are moderate users. On occasions when mothers use a lot of caffeine, however, their nursing infants may be fussier and have more trouble sleeping. This substance is the first synthetic central nervous system depressant, created in the 1830s. After that creation, however, several decades passed be- fore chloral hydrate’s medical usage as a sleep inducer began. In the nineteenth century the drug was popular among middle-class women and middle-aged men for reducing anxiety. In former times chloral hydrate was routinely administered to produce an- esthesia, but such use is tricky; the difference between an effective dose and a poisonous one is so close that the drug has been replaced by other substances for human anesthesia, although chloral hydrate is still used for that purpose in animals. The substance has been largely superseded by barbiturates but still has medical applications as a sedative and to induce sleep. Chloral hydrate is also used to treat seizures caused by fever and is a secondary choice for con- trolling the seizures of status epilepticus (an emergency in which persons keep having epileptic seizures, one after another, with little or no letup). The famed “Mickey Finn” drug used by criminals to knock out victims was a combination of chloral hydrate and alcohol, but animal and human experiments have failed to demonstrate that the combi- nation worked as advertised. The same research, however, also showed that if the product was taken to induce sleep the night before, persons performed better the next day after the drug had worn off, presumably because they were better rested than usual. At normal 80 Chloral Hydrate doses gastrointestinal distress may occur, and persons suffering from stomach irritation are supposed to avoid the compound. A case report notes a delib- erate overdose that destroyed part of a patient’s stomach. In high quantities the compound interferes with heart rhythm and reduces blood pressure and breathing; seizures are possible. Experiments using chloral hydrate on rats and mice have injured the liver, and inhaling the drug’s vapor has caused lung damage in mice. The substance is suspected of causing kidney damage and colon cysts and of aggravating a disease called porphyria. Although the substance is a de- pressant, some persons are stimulated by the drug. In the 1800s a number of prominent persons became addicted to chloral hydrate: English poet and painter Dante Gabriel Rossetti, German literary figure Karl Ferdinand Gutzkow, and renowned German philosopher Friedrich Wilhelm Nietzsche. Such addiction grew uncommon in the twentieth century as the drug itself grew less common. As is so often the case with drug abuse, chloral hydrate addicts were typically polydrug abusers, often using alcohol, opium,ormorphine as well. Today chloral hydrate does not seem to be a popular recreational intoxicant, quite possibly because the kind of person who would enjoy chloral hydrate may instead be attracted to barbiturates, a type of drug that was unavailable in the nineteenth century. No dependence developed after experimenters gave chloral hydrate to mon- keys twice a day for six weeks, but tolerance and dependence can develop in humans. Chloral hydrate withdrawal symptoms include tremors, worry, sleeping difficulty, confusion, delirium, hallucinations, and convulsions. Actions of anti–blood clotting medicines may be tem- porarily boosted by chloral hydrate, but the amount of change and its medical significance are disputed. The drug may reduce blood levels of the epilepsy medicine phenytoin, thereby impeding phenytoin’s therapeutic actions. In mice experimentation chloral hydrate had inconsistent impact on alcohol blood level (sometimes raising it, sometimes reducing it) but extended the time that intoxication lasted. In humans the combination produces changes in heart rate and blood pressure that might harm cardiac patients (the face and neck of one volunteer turned reddish purple from the combination). Alcohol and chloral hydrate are both depressants, and taking them together is like taking an extra dose of one or the other. Lab tests of chloral hydrate’s potential for causing cancer have pro- duced mixed results. The compound has increased the liver cancer rate in mice, but skepticism exists about human relevance of those mice results be- cause dosage was long term and so high as to be poisonous—circumstances not at all similar to an occasional normal therapeutic dose. Experimenters administered the substance to hundreds of rats every day for over two years Chloral Hydrate 81 without evidence developing that the drug causes cancer. Chloral hydrate passes from a pregnant woman into the fetus but is not considered a cause of birth defects. Infants born to such women are, however, more likely to have a condition called hyperbilirubinemia, which can lead to jaundice. Some investigators also believe that administering the drug to infants after birth causes hyperbilirubinemia. The compound passes into the milk of a nursing mother, enough to slightly sedate the infant. Chlordiazepoxide was the first benzodiazepine tranquilizer and has been commonly used since 1960. It is considered one of the safer psychiatric drugs and has actions comparable to those of barbiturates and alcohol. This classic benzodiazepine is used mainly for calming anxiety and for treat- ing symptoms of alcohol withdrawal, including delirium tremens.

However cheap aciphex 20 mg without a prescription gastritis high fat diet, preterm delivery and 308 Substance abuse during pregnancy perinatal mortality were increased in frequency (Eriksson et al cheap aciphex 20 mg gastritis diet . Follow-up of these children found that 15 percent were delayed in academic achievement in school aciphex 10mg fast delivery gastritis symptoms treatment diet, but other adverse effects were not reported (Eriksson et al buy cheap aciphex 10 mg on-line chronic gastritis raw vegetables. Medically supervised use of amphetamines during pregnancy is not convincingly asso- ciated with an increased frequency of congenital anomalies among several thousand infants exposed during the first trimester (Heinonen et al. Illegal metham- phetamines are known as ‘designer drugs’ because they are synthesized by methylating novel sites along the carbon chain and ring in a one-step reduction process. Sometimes methamphetamines are used to ‘cut’ or dilute other illicit drugs (cocaine). In 2006, they are called ‘club drugs’ because they are available in night clubs, and are used in parties called ‘raves’ that may last 24 hours or longer. The stimulant effects of methamphetamines keep the party-goers awake, although some vari- eties of this drug may cause hallucinations or other altered states of consciousness. Notably, the prevalence of methamphetamine use has not decreased over the past decade (Buchi et al. We reported 52 pregnancies complicated by methamphetamines finding that symmetric fetal growth retardation was increased above controls. The frequency of congenital anom- alies was not significantly increased (Little et al. Perinatal infant abnormalities and maternal pregnancy complications were not increased in frequency. The small sample size of the metamphetamine-exposed groups limits the ability to extrapolate these findings. Methamphetamines and cocaine use in pregnancy were associated with lower birth weight but not with anomalies (Oro and Dixon, 1987; Chomchai et al. Fetal growth retardation was associated with methamphetamine use throughout pregnancy, but when drug use was discontinued after the second trimester no difference in birth weight was found (Smith et al. Cannabinoid use during pregnancy 309 Lower birth weight was associated with maternal methamphetamine use during pregnancy among 47 infants in a study from Thailand (Chomchai et al. Medically supervised use of methamphetamines among 89 infants born to women who took the drug during the first trimester reported a frequency of congenital anom- alies no different from controls. Among 320 infants born to women who used the drug after the first trimester there were no abnormalities (Heinonen et al. The rele- vance of medically supervised use of methamphetamines to abuse employing much higher doses is not possible to assess. Frequencies of congenital anomalies (brain, anencephaly, eye, cleft palate) were increased among mice and rabbits whose mothers were given methamphet- amines during pregnancy at doses up to 20 times the therapeutic adult human dose (Kasirsky and Tansy, 1971; Martin et al. Summary of amphetamine/methamphetamine use Medically supervised use of amphetamines and methamphetamines during pregnancy does not seem to pose significant risks for increased frequencies of congenital anomalies or maternal–fetal complications. Risks for congenital anomalies and pregnancy compli- cations for those who abuse this class of drugs may exist and probably involve serious complications secondary to vascular disruption and other cardiovascular accidents. Estimated prevalence rates of cannabinoid use during pregnancy vary widely, ranging from 3 to more than 20 percent of gravidas. Prolonged labor and meconium-stained amniotic fluid apparently increased in frequency in one uncontrolled study of 35 women who smoked marijuana late in pregnancy (Greenland et al. Perinatal infant effects Significantly lowered birth weights have been reported among infants whose mothers used marijuana during pregnancy in three studies (Cornelius et al. Among more than 1200 infants whose mothers smoked marijuana during pregnancy, 137 during the first trimester, the frequency of major congenital anomalies was not increased (Linn et al. Although not generally accepted, a syndrome (fetal growth retardation, craniofacial and other minor dysmorphologic features) was proposed in a clinical case series that included five infants born to women who used two to 14 joints (cigarettes) of marijuana daily throughout pregnancy (Qazi et al. The infants probably had fetal alcohol syndrome and this finding has not been replicated. Most animal teratology studies of marijuana are negative, particularly if dosing (amount, route of intake) was comparable to the human situation. Withdrawal symptoms Among infants born to women who used marijuana near the time of delivery, certain neonatal neurobehavioral abnormalities (tremulousness, abnormal response stimuli) were found (Fried, 1980; Fried and Makin, 1987), but other studies found no differ- ences (Tennes et al. Summary of cannabinoid use Mild fetal growth retardation and maternal lung damage are the only untoward out- comes that can reasonably be attributed to marijuana use during pregnancy. Importantly, woman who use marijuana during pregnancy frequently use other sub- stances know to be harmful substances (i. It is an epidemic that began in the mid to late 1970s and has reached users of virtually every age, sex, ethnic, and socioeconomic subgroup. The use of cocaine is accepted to be dangerous to intrauterine development and can cause birth defects (not a syndrome), fetal growth retardation, and transient withdrawal symptoms. Postnatal intellectual development also seems to be adversely affected by the drug. Cocaine use among pregnant women We first estimated the prevalence of cocaine use during pregnancy at 9. Survey results in public hospitals range from 11 to 31 percent (Brody, 1989; Nair et al. Much of the professional community was unprepared to deal with the large number of cocaine-exposed fetuses over the last decade (Landry and Whitney, 1996; Kuczkowski, 2005). In one study, approximately 77 percent of pregnant cocaine abusers at a large public hospital used other drugs of abuse and/or alcohol (Little et al. We found that cocaine crosses the placenta and is metabolized in the placenta through plasma cholinesterase to ecgonine methyl ester, a major active metabolite (Roe et al. Coronary artery vasospasm and arrhythmias occur at even very low doses of cocaine (Lange et al. Chronic cocaine use can lead to myocardial infarction, congestive heart failure, dilated cardiomyopathy, or severe ischemic events in the heart or brain (Box 16. In more severe situations, cocaine can aggravate vascular weakness and cause serious vascular accidents (intracerebral infarctions and hemorrhages, acute ischemic brain events). Death from cocaine toxicity is usually preceded by hyperpyrexia, shock, unconsciousness, respiratory/cardiac depression. Chronic cocaine use is associ- ated with epileptogenic seizures and cerebral atrophy (Pascual-Leone et al. Maternal cocaine use during pregnancy was associated with significantly shortened mean gestational periods and increased frequencies of preterm labor (Chasnoff et al. This drug is significantly associated with an increased frequency of precipitous labor (Bateman et al. Gestation length and frequency of preterm delivery among women who used only cocaine during the first trimester were not found to be significantly different from women who did not use cocaine during pregnancy (Chasnoff et al. Others have found no association with preterm labor or low birth weight when other obstetric complications were con- trolled (Miller et al. However, other risks (birth defects, low birth weight, prematurity, decreased length, and lower head circumference) were said to be related to polydrug use, and could not be attributed to cocaine use (Addis et al. Cerebrovascular accidents and related cocaine toxicity Fatalities following adult cocaine use have frequently been reported. However, only four cases have been documented that involve pregnant women (Burkett et al. Of the published cases, two were due to subarachnoid hemorrhage resulting from ruptured aneurysms and a third case involved a pregnant woman admitted to the hospital in a comatose condition after about 1. She was maintained on life-support sys- tems and eventually died approximately 4 months later, never having regained conscious- ness. The fourth maternal death was attributed to cardiac ischemia and arrhythmia (Burkett et al. Among more than 4 million women studied in California, the risk of maternal mortality was more than doubled among women who used cocaine during pregnancy (Wolfe et al.

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Inspect visually for particulate matter or discoloration prior to administration and discard if present aciphex 10mg on-line gastritis prognosis. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present aciphex 20 mg with visa chronic gastritis lasts. Technical information Incompatible with No information Compatible with Flush: NaCl 0 buy aciphex 20mg free shipping gastritis diet . Additional information Common and serious Immediate: Anaphylaxis and other hypersensitivity reactions may occur proven aciphex 10 mg gastritis poop. This assessment is based on the full range of preparation and administration options described in the monograph. Its use arises from the property of cobalt salts to form a relatively non-toxic stable ion-complex with cyanide. Dicobalt edetate is toxic and potentially fatal in the absence of cyanide poisoning. Pre-treatment checks * Must only be used in cases of confirmed severe cyanide poisoning. If the patient is fully conscious, it is unlikely that the extent of poisoning warrants the use of dicobalt edetate injection. Biochemical and other tests Nil Doses of cyanide poisoning antidotes1 (see relevant entries) Itisessentialtoconsult apoisonsinformationservice,e. Severe poisoning (coma, fixed dilated pupils, cardiovascular collapse, respiratory failure, cyanosis): If dicobalt edetate is available: As well as other supportive measures: * Give 300mg (20mL) of 1. If a second dose of dicobalt edetate is given, there is "risk of cobalt toxicity but only if the diagnosis is not cyanide poisoning. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Technical information Incompatible with Not relevant Compatible with Not relevant pH 4--7. Dicobalt edetate | 245 Monitoring Measure Frequency Rationale Signs of Throughout treatment * May cause anaphylactoid reactions, particularly hypersensitivity in overdose (or in the absence of cyanide). Additional information Common and serious Immediate: Anaphylactic reactions including facial and laryngeal oedema undesirable effects (facilities for intubation and resuscitation should be immediately available). This assessment is based on the full range of preparation and administration options described in the monograph. Wolff--Parkinson--White syndrome; ventricular tachycardia or fibrillation; hypertrophic cardiomyopathy (unless concomitant atrial fibrillation and heart failure -- but with caution). The dose may alternatively be given in divided doses, each over 10 to 20 minutes, with about 50% of the total dose given initially and additional fractions (usually 25%) given at intervals of 6 to 8 hours if still indicated. Commence oral maintenance therapy on the following day adjusted according to age, lean bodyweight and renal function. If the patient is already maintained on digoxin convert directly from previous oral maintenance dose (see below). Dose in renal impairment: consider reducing maintenance dose and monitoring levels if CrCl <50mL/minute. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. For loading doses only, where a fraction is to be given, this may be infused over 10 to 20 minutes. Technical information Incompatible with Amiodarone, amphotericin, fluconazole, foscarnet, insulin (soluble), propofol. Contains propylene glycol (adverse effects seen in #renal function, may interact with disulfiram and metronidazole). Stability after From a microbiological point of view, should be used immediately; however, preparation prepared infusions may be stored at 2--8 C and infused (at room temperature) within 24 hours. Monitoring Measure Frequency Rationale Heart rate Priortoloadingdoses * Ventricularrateshouldnotbeallowedtofallbelow and if at risk of #pulse 60 bpm except in exceptional circumstances, e. Serum digoxin If there are signs or * A blood sample should be taken a minimum of 6 concentration symptoms of toxicity. Additional information Common and serious Infusion-related: Too rapid administration: heart block, life-threatening undesirable effects arrhythmias, death. Other: #Pulse, arrhythmias, nausea, vomiting, diarrhoea, dizziness, blurred or yellow vision, skin rashes. Pharmacokinetics Elimination half-life is 20--50 hours; longer in renal impairment. Action in case of Symptoms to watch for: In massive overdose progressive "K occurs (fatal unless overdose reversed), arrhythmias. Antidote: Life-threatening overdose may be treated with digoxin-specific antibody fragments(see Digoxin-specificantibody fragmentsmonograph). Digoxin-specific antibody fragm ents (Digibind, F(ab)) 38-mg dry powder vials * Digoxin-specific antibody fragments are derived from sheep immunised to digoxin. Standard digoxin serum assays cannot be used to determine free, pharmacologically active digoxin after administration of Digibind because these also detect F(ab)-bound digoxin. Pre-treatment checks * Previous exposure: Although allergic reactions have been reported rarely, patients known to be allergic to sheep protein and patients who have previously received digoxin-specific antibody fragments are likely to be at greater risk of developing an allergic reaction. Inaccurate serum digitalis con- centration measurements are a possible source of error; this is especially so for very high values, since most digoxin assay kits are not designed to measure values >5 nanograms/mL. Acute ingestion of an unknown amount of cardiac glycoside where serum concentra- tion is not available: 10 vials can be administered followed by an additional 10 vials if clinically indicated. Dose ðnumber of vialsÞ¼Total body load ðmgÞ* Â 2 *Total body load is either (dose in mg of digoxinÂ0. Table D4 Estimated dose of Digibind to treat acute ingestion of a known quantity of digoxin Number of 250-microgram digoxin Digibind dose tablets (number of vials) (80% bioavailability assumed) 25 10 50 20 75 30 100 40 150 60 200 80 Toxicity during chronic therapy where serum concentration is not available: 6 vials will usually be adequate to reverse toxicity. Toxicity during chronic therapy where serum concentration is available: For digoxin toxicity: if serum concentration is known, use the following formulas to calculate number of vials needed. Serum digoxin concentration ðnanograms=mLÞÂbodyweight ðkgÞ Dose ðnumber of vialsÞ¼ 100 For digitoxin toxicity: Serum digitoxin concentration ðnanograms=mLÞÂbodyweight ðkgÞ Dose ðnumber of vialsÞ¼ 1000 Intravenous infusion (preferred method) Preparation and administration 1. Withdraw the contents from the required number of vials and add to a convenient volume of NaCl 0. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. T able D stim ated ofn um bervial sofD igibin d required fora kn ow serum digox in con cen tration S erum di g oxi nconcentrati on B odyw ei g h t nanog ram s/ ( kg ) m i crog ram s/ L nanom ol N um berof v i als 4 6 7 8 1 252 | Digoxin-specific antibody fragments Intravenous injection (if cardiac arrest seems imminent) Preparation and administration 1. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. Technical information Incompatible with No information Compatible with Flush: NaCl 0. Displacement value Not relevant Stability after The product should be used promptly after preparation. However, reconstituted preparation vials may be stored at 2--8 C for up to 4 hours if necessary. Monitoring Measure Frequency Rationale Signs of clinical Shortly after * If after several hours toxicity has not adequately improvement administration reversedorappearstorecur,re-administrationata dose guided by clinical judgement may be required. Serum K Every 1--3 hours until * Severe digitalis intoxication can cause life- serum K is stabilised threatening "K concentration by shifting K from within the cells. Digoxin-specific antibody fragments | Dihydrocodeine tartrate | 253 Additional information Common and serious Injection-related: Too rapid administration: Although rare, allergic undesirable effects reactions are thought to be more likely with rapid dosing. Signs and symptoms of digitalis intoxication should begin to improve within 30 minutes of administration.

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At a constant preload in the isometrically contracting muscle purchase 20 mg aciphex otc gastritis y dolor de espalda, max dF/dt is an excellent index of contractile state when testing the effects of different drugs order 10mg aciphex mastercard gastritis symptoms remedy. However discount aciphex 20 mg with visa gastritis diet , max dF/dt does change somewhat with changes in preload discount 10mg aciphex with visa gastritis video, so that it is not totally specific for contractile state alone. The same is true for V max which is altered substantially by changes in contractility and slightly by changes in preload. On the other hand, the total force line is more specific for changes only in contractile state. Table 3 has paired some of the analogous terms which are used in isolated heart muscle and in the intact heart. In isolated heart muscle we measure force, whereas in the intact heart we measure intraventricular pressure. Force in the wall of the heart is related to pressure by the Laplace relation, a simplified form of which is shown in the table. The passive length-tension curve of isolated muscle and the passive pressure volume relation of the left ventricle are both exponential curves which resist further lengthening at higher force or pressure. The term preload refers to the initial load stretching isolated heart muscle prior to contraction. In isolated heart muscle, the afterload refers to the additional load above the preload which the muscle has to match in order to shorten. In an analogous way, the aortic pressure represents the pressure that must be developed by the left ventricle before it can open the aortic valve and eject blood. The active length-tension curve has a somewhat similar shape to the ventricular function curve illustrated in Figure 20. These pressures represent the diastolic filling pressure of the left ventricle, and thus are an index of preload. A normal left atrial pressure is generally less than 12 mmHg, so that the heart is normally working on the ascending limb of the left ventricular function curve. The pulmonary capillary wedge pressure is an approximation of the left atrial pressure (and therefore of left ventricular end-diastolic pressure). By definition, the ejection fraction is the stroke volume divided by the end-diastolic volume. In principle, this is conceptually related to a ventricular function curve, as illustrated in Figure 21. By plotting stroke volume versus the end-diastolic volume, different curves of left ventricular performance are illustrated. As left ventricular performance decreases, ejection fraction is reduced and the ventricular function curve is shifted down and to the right (A to B to C). The ejection fraction is one of the most useful single numbers for characterizing left ventricular performance (although it is load-dependent). The ejection fraction is the slope of the dashed line connecting the origin to points A, B, and C on the three different curves. As the curves are progressively shifted down and to the right to a lower level of function, there is a decrease in the ejection fraction. During the process of heart failure, there are three immediate compensatory mechanisms used to maintain cardiovascular compensation. These are (1) dilation (Frank-Starling mechanism), (2) sympathetic stimulation and an increase in circulating catecholamines, and (3) increased heart rate. The effect of two of these mechanisms on the ventricular function curve is shown in Figure 22. During the process of heart failure, the left ventricle has moved from point A on the normal curve down to point B on a depressed and failing curve. Since cardiac output is the product of stroke volume and heart rate, an increase in heart rate will also tend to maintain cardiac output when stroke volume is reduced. Chronic compensatory mechanisms include (1) hypertrophy, which occurs with both volume and pressure overload, and (2) increased extraction of oxygen from the blood. This latter effect increases oxygen delivery to body tissues at a given cardiac output. The patient begins at point A on a normal ventricular function curve and shifts down to point B with the development of heart failure. The responses of the ventricle to volume or pressure overload are shown in Figures 22 and 23. The passive-pressure volume relations of the ventricle are usually altered by pressure or volume overload (Fig. In volume overload such as occurs with aortic or mitral valvular regurgitation, the ventricle tends to dilate and the curve is shifted to the right with an increase in compliance. In pressure overload such as occurs with aortic stenosis, the curve is often shifted to the left. The wall hypertrophies with a reduction in intraventricular volume (decreased compliance). Figure 23: Changes in the passive-pressure volume relation of the ventricle in response to volume overload (increased compliance) and pressure overload (decreased compliance). An important principle relating to the onset of heart failure is that there may be preservation of ventricular function at rest although the reserve of the heart in response to stress or exercise is markedly reduced. In response to an increase in arterial pressure, there is a tendency for stroke volume to be reduced because of the increased afterload. The ventricle, therefore, increases its contractility by responding to increased systemic and local norepinephrine secretion to maintain stroke volume. This results in a shift upward in function as shown by the dashed line (A) to the higher function curve. This represents a normal integrated response to an increase in arterial pressure in a compensated ventricle. The upper control curve of patient B has resting measurements similar to the resting measurements of patient A. In response to the same increase in arterial pressure, however, this patient has little reserve. Therefore, as afterload is increased, there is a reduction in left ventricular performance and cardiac dilation. This results in a marked shift of function down and to the right (dashed line), as illustrated. Thus, although resting measurements of performance were similar in the two patients, patient A had relatively normal ventricular reserve, whereas patient B had a marked reduction in ventricular reserve. Patient B, therefore, would probably also be limited by symptoms of shortness of breath and fatigue during exercise. It appears that some depletion of high energy phosphates may occur in heart failure, although this is probably not the cause of the heart failure. The oxygen consumption of the heart has an important relationship to pressure development and to shortening. As a general rule, pressure development requires more oxygen than does shortening. Therefore, increases in stroke volume require less of an increase in oxygen consumption than an increase in pressure development. The major determinants of myocardial oxygen consumption are: heart rate, left ventricular pressure, heart size, and contractile state. When any or all of these are increased, there is an increase in oxygen consumption. Minor determinants of oxygen consumption include the basal levels required to maintain cellular integrity, the minor cost of activation, and the direct metabolic effects of catecholamines. Cardiac muscle can increase its performance by an increase in muscle length and/or an increase in contractile state. The primary determinants of myocardial performance are preload, afterload, contractile state, and heart rate.

By H. Thorald. Christopher Newport University.

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