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By L. Javier. Towson University.

However cheap accutane 10mg with mastercard, cost data are occasionally collected from patients to obtain cost information that is relevant to the patient (e cheap accutane 30 mg fast delivery. The key to obtaining cost data from patients is to ensure that the questions asked are clear generic accutane 10mg online, easy to read purchase accutane 5 mg with mastercard, and understandable. Additionally, other relevant cost information must be collected as needed from other sources (e. In the past decades, economic evaluation has been increasingly important for the decision maker to decide which treatment or intervention is more cost-effective in order to allocate limited health-care resources soundly. The aim of economic evaluation is to compare interventions in terms of their costs and benefits, including their patient outcome impact. Once the need for the measure is recognized, its purpose and clinical usefulness 172 need to be considered in order to inform the validation design. For example, a symptom measure would be developed and validated differently from a treatment satisfaction measure because of the different concepts evaluated by these outcomes. In addition to obtaining clinician input and reviewing the literature to better understand the disease, questionnaire items should be developed based on carefully planned qualitative research with patients [35–37]. Qualitative research is critical to documenting the content validity of an instrument. Content validity refers to the qualitative assessment of whether the questionnaire captures the range of the concept it is intended to measure among the patient population for which it is intended [38]. For example, does a measure of symptom severity capture all the symptoms that patients with a particular condition have, and if so, is the measure capturing the items in a manner meaningful to patients? To obtain content validity, patients (and clinical experts to some extent) review the measure and judge whether the questions are clear, unambiguous, and comprehensive [7]. Qualitative research methods typically involve focus groups, semi-structured one-on-one interviews, and cognitive interviews [1,37,39]. Focus groups, which typically involve six to ten people with a common attribute, such as a disease, can have advantages over individual interviews in that descriptions of the patient experience are enriched by participants’ responses to the comments of others [7]. Conversely, personal or sensitive topics may be better suited for one-on-one interviews or gender- specific groups. Focus groups and one-to-one interviews should be conducted by moderators with experience in qualitative methods, following a semi-structured interview or discussion guide. Data collected at this stage can be used to determine the relevance of concepts to patients. Building on this, developmental focus groups are designed to explicitly capture patient descriptions of the proposed concept of measurement, including the themes, topics, and language that patients use in describing their experience. Careful consideration at this point should be given to the questionnaire intent and purpose [35]. For example, if a measure is intended to assess symptom bother, interview questions should be designed to elicit the words and phrases patients use to describe the impact of their condition. Rather than using clinical terminology that patients may not understand, the words used during the focus groups or interviews should be common to patients. Moderator prompting should be designed to elicit emergent information rather than leading participants to prespecified responses. Finally, evaluative or confirmatory focus groups or interviews can be conducted to provide documentation that an existing instrument is appropriate for a given purpose and patient population. Qualitative data obtained in confirmatory focus groups can be used to map content, words, phrases, and themes to items from existing and/or newly developed instruments. Saturation is defined as the point at which no substantially new themes, descriptions of concepts, or terms are introduced as additional focus groups or interviews are conducted [40]. The exact number of focus groups or interviews needed to reach saturation is determined by the number of concepts elicited, the complexity of these concepts, and the attributes of the patient population (e. After questionnaire items have been generated, the newly drafted questionnaire should be reviewed by other patients and experts to ensure its readability and provide additional evidence of content validity. Cognitive interviews are one-on-one interviews designed to uncover problems in the social- cognitive processes involved in completing a questionnaire [41]. During cognitive interviews, patients are typically asked to review and respond to the questionnaire items and are then interviewed about what each item meant to them as they completed the questionnaire. The results are used to make modifications in the words or phrases in the items, response options, recall period, and instructions or format of the instrument in order to improve ease of administration and enhance the validity [7]. This process is also important when reviewing or adapting an existing measure to meet the needs of a new patient population. The adapted questionnaire must be validated on its own in the target population; the validity of the original questionnaire does not apply to an adapted measure. Saturation should be demonstrated in the cognitive interviewing process in a similar way to that used in the initial focus group or one-on-one interview process used to generate items. Also valuable for content validity review is a listing of all changes made to each item in the 174 instrument development process, the rationale for decisions to drop or change items, and a record of items added or dropped [2]. Determining the Mode of Administration of a Questionnaire Once items have been generated, the mode of administration must be considered. How the questionnaire will be completed needs to be determined before the validation stage because the mode of administration can affect patient responses. For highly personal or intimate questions or questions regarding satisfaction, a self-administered questionnaire is recommended to avoid response bias. Questionnaires that are self-administered are preferable to interviewer- administered questionnaires because the data collection burden is reduced and patients are more likely to provide unbiased information on self-administered questionnaires. Importantly, if a questionnaire has been validated for a particular mode of administration, this does not make the questionnaire valid for all modes of administration. This applies to varying modes of self-administration such as going from pen and paper to electronic; the new mode of administration needs to be demonstrated as equivalent to the initial mode of administration. Perform a stand-alone cross-sectional study to validate the questionnaire in the patient population for which it was designed. Administer the untested questionnaire in a clinical trial and use the baseline data to perform psychometric validation (the end-of-study data can also be used to evaluate responsiveness). Perform a stand-alone longitudinal study with an intervention to determine the instrument’s psychometric performance and responsiveness in a nonclinical trial setting. The following psychometric properties must be tested for and demonstrated in a validated questionnaire: Reliability refers to the ability of a measure to produce similar results when assessments are repeated (i. Reliability is critical to ensure that change detected by the measure is due to the treatment or intervention and not due to measurement error [43]. Test–retest reliability, or reproducibility, indicates how well the results can be reproduced with repeated testing. To assess test–retest reliability, the same patient completes the questionnaire more than once, at baseline and again after a period of time during which the impact of symptoms is unlikely to change (e. The Spearman’s correlation coefficient and intraclass correlation coefficient are used to demonstrate reproducibility. For group data, a Spearman’s correlation coefficient or an intraclass correlation coefficient of at least 0. Internal consistency reliability is another measure of reliability that indicates how well individual items within the same domain (or subscale) correlate [42,45]. Cronbach’s alpha coefficient is used to assess internal consistency reliability, with higher alphas indicating greater correlation [46,47]. Interrater reliability indicates how well scores correlate when a measure is administered by different interviewers or when multiple observers rate the same phenomenon [42]. Demonstration of interrater reliability is not necessary for self-administered questionnaires but is necessary for instruments based on observer ratings or using multiple interviewers. Validity refers to the ability of an instrument to measure what it was intended to measure [3,42,43]. A measure should be validated for each specific condition or outcome for which it will be used. Evidence of content validity, convergent validity, discriminant validity, and criterion validity typically are required to validate a questionnaire [42]. As described previously in relation to qualitative research, content validity is a qualitative assessment of whether the questionnaire captures the range of the concept it is intended to measure. Construct-related validity refers to evidence that an instrument behaves in a way that is consistent with the theoretical implications associated with the constructs being measured [3]. Convergent validity is demonstrated by the extent to which the measure correlates with other measures designed to assess similar constructs [49]. Discriminant validity refers to the degree to which the scale does not correlate with other measures designed to assess dissimilar constructs or is able to discriminate between constructs that should be related [49]. Stronger relationships should be seen with the most closely related constructs and weaker relationships seen with less-related constructs [43]. Another common method for examining construct-related validity is to evaluate whether a questionnaire can differentiate between known patient groups (e. Criterion validity reflects the correlation between the new questionnaire and an accepted reference or gold standard [3,51]. One difficulty in establishing criterion validity is that a gold-standard measure might not be available [3]. When criterion validity can be established with an existing measure, the correlation should be 0. Responsiveness indicates whether the measure can detect change in a patient’s condition [3,43]. An important aspect of responsiveness is determining not only whether the measure detects change but whether the change is meaningful to the patient. A measure that is valid and reliable for a particular language and culture may not prove so when used in a different population. Linguistic and cultural adaptation of a questionnaire occur during the development phase before validation, or it can be done after the questionnaire is validated in the language in which it was initially developed, with the latter being the more common approach. Ensuring the linguistic and cultural validity of a questionnaire is especially important for measures used in multinational clinical trials. The principal steps in adapting a measure for different languages and cultures are as follows: 1. Quality-control procedures that may include a backward translation (translating the instrument back into the original language) [58] 3. Discussion by an expert panel to ensure clarity of the translated questionnaire 5. Testing the translated instrument in monolingual or bilingual patients to ensure that it measures the same concepts as the original instrument [45,56,58] 176 However, if a backward translation of the measure does not produce a semantically equivalent instrument, then the instrument may need to be developed in the target language, rather than just translated [58]. Thus, reliability, validity, and responsiveness need to be assessed with each language translation to confirm the same measurement properties are present in the translated language(s) to ensure psychometric equivalence. As such, a new questionnaire or modifications to an existing questionnaire may be needed that would require additional investigation and to establish relevance and content validity among the specific patient group. Importantly, any modifications of established questionnaires may result in changes (sometimes substantial) in the psychometric performance of the instrument. Consequently, all modified instruments should be qualitatively reviewed first by the target patient population to ensure patient understanding and relevance as well as be subjected to the same psychometric testing as that employed in developing a completely new instrument.

Refractoriness of S3 now depends on previous diastolic interval (80 msec) purchase accutane 30mg without a prescription, as well as a refractory period of S2 (which is shorter than the refractory period of S1) 5mg accutane sale. This results in a refractory period of S3 at an S1-S2 = S2-S3 of 260 msec that is 195 msec order 30mg accutane amex. This compares to a refractory period of 220 msec during the drive and a ventricular refractory period of S2 of 180 msec buy generic accutane 5 mg line. Shortening of ventricular refractorines with extrastimuli: Role of the degree of prematurity and number of extrastimuli. A wide range of normal values has been reported for refractory periods (Table 2-5). The data would be more meaningful if they were all obtained at comparable cycle lengths using the same stimulus strength and pulse width. In these different laboratories, stimulus strengths vary from twice threshold to 5 mA, and pulse widths vary from 1 to 2 msec; both of these factors can alter the so-called normal value. As noted previously, strength–interval curves may be the best way to determine atrial and ventricular refractoriness. Another factor affecting the validity of such “normal” data is that A-V nodal conduction and refractoriness are both markedly affected by autonomic tone, an impossible factor to control except by autonomic blockade, which is not done routinely. Although atrial, ventricular, and His–Purkinje refractory periods appear relatively independent of autonomic tone and are therefore relatively stable, A-V nodal refractory periods are labile and can vary significantly during the course of a single study. Although it is difficult to assess the clinical significance of his findings, Prystowsky has shown that enhanced parasympathetic tone shortens atrial refractoriness and prolongs right ventricular refractoriness. The effect of drive cycle length on ventricular refractoriness in any given patient may represent a means of discriminating between abnormal and normal refractoriness when the absolute value of a single refractory period determination is borderline. Dispersion of Refractoriness Dispersion of ventricular refractory periods has been suggested as an indicator of an arrhythmogenic substrate based on animal experiments. For example, ischemic tissue appears to have longer refractory periods than nonischemic tissue. We recently evaluated whether or not dispersion of refractoriness is a measurable entity that has clinical relevance in humans. In a small number of patients, we evaluated differences in dispersion of refractoriness during atrial pacing and ventricular pacing at 600 and 400 msec. We also assessed the difference in dispersion of refractoriness when refractory periods are determined at both twice threshold and at 10 mA (in our experience this is always on the steep portion of the strength–interval curve). Thus, we evaluated both dispersion of refractoriness and dispersion of recovery (local activation plus local refractoriness) at each site. In five patients, we studied the effect of drive cycle length on dispersion of refractoriness. At a paced cycle length of 600 msec, the dispersion of refractoriness was 66 ± 41 msec, and it was similar at a paced cycle length of 400 msec at 65 ± 45 msec. Total dispersion of recovery was 89 ± 40 msec at a paced cycle length of 600 and 88 ± 38 msec at a paced cycle length of 400 msec. Of note, the maximum dispersion at any two adjacent sites of refractoriness was 33 ± 12 msec, and for total recovery it was 41 ± 15 msec. Thus, in our studies,43 cycle lengths from 600 to 400 msec did not alter dispersion of refractoriness, as seen in experimental studies. In these patients we found no significant difference in dispersion of refractoriness. The dispersion of refractoriness was 62 msec at twice threshold and 50 msec at 10 mA, and the total recovery was 79 msec at twice threshold and 68 msec at 10 mA. A limitation of these preliminary data is that in these patients, dispersion measurement methods were mixed, some having twice threshold and 10 mA performed at sinus rhythm and some during a different ventricular-paced cycle length. The difference between this study and our data43 probably relates to the fact that we could not compare very slow rates with faster rates and only studied rates of 100 and 150 bpm in detail. Moreover, the effect of chronic bradycardia and subsequent ventricular enlargement may play an important role in refractory period measurements. Other workers have looked at the effect of site of pacing on refractoriness, considering, for example, whether atrial pacing differed from ventricular pacing. In contrast, when we compared dispersion of refractoriness and recovery from multiple left ventricular sites measured during atrial pacing and ventricular pacing at the stimulation site in five patients, we found no significant difference in dispersion of refractory periods of total recovery times. The difference between these results is unclear, although the small number of pacing sites in the study by Friehling et al. Our data on normal left ventricular dispersion of refractoriness and total recovery time serve as a reference for evaluating the role of dispersion refractoriness and/or recovery in arrhythmogenesis. The signals recorded are quite comparable to intracellular microelectrode recording, and if properly done are stable for a few hours. Thus, the value of this technique in abnormal tissue or in the presence of Na channel blockers is uncertain. Patterns of Response to Atrial Extrastimuli Several patterns of response to programmed atrial extrastimuli are characterized by differing sites of conduction delay and block and the coupling intervals at which they occur. Although it has been stated that any prolongation of His–Purkinje conduction is an abnormal response, it is not. Previous studies demonstrated that 15% to 60% of normal patients can show some prolongation of the H-V interval in response to atrial extrastimuli. Thus, block below the His bundle in response to an atrial extrastimulus delivered during sinus rhythm may be a normal response. The curves may be drawn in two ways: (a) by plotting A1-A2 versus H1-H2 and V1-V, which gives the functional input–output relationship between the basic drive beat and the premature beat, and (b) by plotting the actual conduction times of the premature beat through the A-V node (A2-H2) and His–Purkinje system (H1-V2) versus the A1-A2 intervals. A2-H2 and H2-V2) allows a purer evaluation of the response to A2 because, unlike the former curve, the results are not affected by conduction of the basic drive beat. This becomes particularly important when the effects of drugs or cycle length on the conduction of premature atrial impulses are being evaluated. During this limited decrease, A-V nodal conduction (A2-H2) and His–Purkinje conduction (H2-V2) are unchanged from the basic drive so that the curve moves along the line of identity. The H1-H2 and V1-V2 curves remain identical, localizing the delay to the A-V node, as shown in the right-hand panel as an increase in the A2-H2 interval without any change in the H2-V2. The curve continues to descend at a decreasing slope as further A-V nodal delay is encountered. At a critical Al-A2 interval, the delay in the A-V node becomes so great that the H1-H2 and V1-V2 intervals begin to increase. The increase in H1-H2 and V1-V2 continues until the impulse is blocked within the A-V node or until atrial refractoriness is reached. A-V nodal conduction (A2-H2) usually is prolonged two to three times control values before A-V nodal block. If the increment in H2-V2 approximates the decrement in A1-A2, V1-V2 assumes a relatively fixed value, producing a horizontal limb. At longer coupling intervals, conduction is unchanged and the curve decreases along the line of identity. Further shortening, however, produces a sudden jump in the H2-V2 interval, resulting in a break in the V1-V2 curve, which subsequently descends until, at a critical Al-A2 interval, the impulse usually blocks within the A-V node or His–Purkinje system. Aberrant conduction invariably accompanies beats with prolonged His–Purkinje conduction times. Again, autonomic tone at the time of catheterization can markedly affect the percentage of patients whose A-V nodes have the longest refractory periods during antegrade stimulation. The cycle lengths at which these refractory period measurements were made were highly variable, and inconsistent use of sedation, I believe, explains the disparate results. Patterns of Response to Ventricular Extrastimuli Retrograde conduction has been less well characterized than antegrade conduction. In patients with A-V dissociation, we employ simultaneous atrial and ventricular pacing during the basic drive to prevent supraventricular captures from altering refractoriness by producing sudden changes in cycle length. Moreover, potential changes in hemodynamics related with A-V dissociation may also affect the reproducibility of refractory period studies. Thus, attention should be given to ensuring a constant 1:1 relationship between ventricular pacing and atrial activation. Similar stimulation methods must be used, therefore, when drug effects or other interventions are to be compared. Although the functional properties of conduction and refractoriness follow principles similar to those of antegrade studies, the most common site of retrograde delay and block is in the His–Purkinje system. Detailed assessment of retrograde conduction was limited in the past by the fact that the His bundle deflection was not uniformly observed during the basic drive, thus making the cases reported relatively selected. More recently, using bipolar electrodes with a 5-mm interelectrode distance and being extremely careful, we have been able to record retrograde His deflections during the ventricular-paced drive in up to 85% of our patients. A second limiting factor is that during ventricular extrastimuli the His deflection can be buried within the ventricular electrogram over a wide range of ventricular coupling intervals, therefore making measurements of ventricle to His bundle conduction times impossible in these circumstances. This technique, although not widely used, offers the best method of evaluating retrograde His–Purkinje conduction during programmed ventricular stimulation. Since a retrograde His potential may not be observed even at close coupling intervals in approximately 15% to 20% of patients using standard techniques (pacing the right ventricular apex), evaluation of His–Purkinje and consequently A-V nodal conduction is at best incomplete. The rationale for choosing S1-H2 is the observation in animals and in occasional patients that over a wide range of ventricular-paced rates, S1-H1 remains constant (Figs. The typical response shown in Figures 2-43 and 2-44 may be graphically displayed by plotting S1-S2 versus P. As noted, the ability to record a retrograde His deflection during the basic drive greatly facilitates analyzing the location of conduction delays and block. Similar retrograde His potentials and retrograde V-A conduction patterns have been observed during left ventricular stimulation (Fig. As the ventricular extrastimuli are delivered at progressively premature coupling intervals (S1-S2), progressive delay in retrograde His–Purkinje conduction (S2-H2) is noted (A, B). On the right, during para-Hisian pacing, a retrograde His is clearly seen prior to the echo beat. B–C: Progressive retrograde His–Purkinje conduction delay appears as S1-S2 shortens. Further shortening results in a decrease in A1-A2 and an increase in S2-A2 intervals. The exact site of this initial delay cannot always be determined because a His bundle deflection may not be observed. In the absence of a recorded retrograde His bundle deflection, the site of initial S2-A2 delay cannot be inferred to be in the A-V node. As S1-S2 is progressively shortened, a retrograde His deflection (H2) eventually appears after the ventricular electrogram recorded in the His bundle tracing. The converse of these observations occurs when stimulation is performed from the left ventricle. The routes of retrograde His–Purkinje conduction just described have been studied in detail by Akhtar et al. Had retrograde His potentials and right bundle potentials been seen during ventricular drive, it is probable that a greater percentage of patients would have had initial conduction over the right bundle with subsequent conduction over the left bundle. In patients who have pre-existent antegrade bundle branch block, retrograde block in the same bundle branch is common. In fact, when pacing is instituted from the ipsilateral ventricle, the V-H interval is usually so long that retrograde Hs, if seen, are usually observed after the local ventricular electrogram. Once a retrograde His bundle deflection is seen, progressive prolongation of His–Purkinje conduction (S2-H2) occurs as the S1-S2 interval decreases.

Te complete cessation of blood fow Te right ventricle pumps blood against a resistance through the ductus venosus occurs by 7th postnatal day which is higher than that of the left ventricle of life 40mg accutane with amex. Te loss of placental fow also results in decrease 464 in volume of blood returning to the right atrium and relationship of pressure and resistance in the pulmonary consequent drop in the right atrial pressure effective 30 mg accutane. Increase and systemic circulation is established in approximately in left atrial pressure results in left atrial pressure being 2–3 weeks trusted 40mg accutane. All these changes result in the establishment higher than the right atrial pressure discount 40mg accutane otc. Te approximation of septum diferent parts of the body through superior and inferior primum with septum secundum contributes to the vena cava reaches right atrium, courses through the right closure of foramen ovale. Tough the functional closure ventricle and through pulmonary vessels to the lungs for of foramen ovale occurs quickly, the anatomical closure oxygenation. Oxygenated blood reaches left atrium, then occurs over a period of months to year. Since its etiology leads to reversal of blood fow through the ductus in infancy and childhood is at considerable variance arteriosus. Instead of fowing from pulmonary trunk with that of adults, the diagnosis as well as therapeutic to aorta, blood starts fowing in the reverse direction. Tough failure means failure on the part of the heart to: the exact mechanism is not known, the musculature Maintain an output necessary for the metabolic of the ductus arteriosus has been found to be sensitive requirements of the body at rest or during stress to change in oxygen saturation. In preterm babies, the functional patience may be precipitated by various Etiology* problems in immediate postnatal period (Box 27. Te pulmonary vascular resistance and right ventricle pressure continue to decline over next few weeks. The complete cessation of blood fow z Excessive perspiration through the ductus venosus occurs by 7th postnatal day of life. The z Hepatomegaly functional closure occurs immediately and anatomical closure occur in months to year. In full z Edema, usually involving eyes, sacrum, legs and term neonates, the ductus arteriosus closes within 10–21 days. Right-sided heart failure be given to control the coexisting infection/suspected z Enlarged tender liver infection that could have precipitated the failure by z Facial pufness increasing cardiac work. Both left and right-sided heart failure z Cardiomegaly Correction of anemia: Blood transfusion (packed z Poor peripheral pulses cells, 3–5 ml/kg), given carefully and slowly, leads to z Cyanosis reduction in cardiac work. Children Vasodilators: Vasodilators such as nitroglycerine and z Dyspnea at rest (orthopnea) or on exertion nitroprusside counter the existing vasoconstriction; z Tachycardia thereby improving cardiac output and reducing work z Raised jugular venous pressure of the heart. Investigations z One-half of the total calculated dose should be Chest X-ray assists in: given stat. Parenteral dose should be about two-thirds Echocardiographyhelps in assessing functional capacity of the oral dose. Nevertheless, in practice, it has been found useful Management and is recommended in all grades of heart failure. Goals It improves the cardiac output, thereby indirectly Reducing cardiac work reducing the systemic impendence. This unloads Increasing myocardial contractility the ventricles, reducing their work. In practice, only dopamine and dobutamine are of z Step 2: Digoxin which improves cardiac contractility by its proven value in pediatric heart failure. Diuretics: Frusemide, in a dose of 1–3 mg/kg orally z Step 6:Beta blockers (propranolol) or steroids if active myocarditis and 0. As yet, fgures on incidence in India are not Triamterene and amiloride may also be used. Increased prognosis, provided that the surgical intervention is energy needs from heart failure needs to be met. Tis, together with the Measures for Correction of the Underlying Cause increasing information regarding its signifcant incidence, Correction of the underlying cause should be seriously highlights that it is worthwhile to make an early diagnosis considered. Surgically treatable causes like valvular lesions, seem to have a defnite bearing. Te z Therapy with a vasodilator nitroprusside, intrave- incidence is higher among siblings. Also, siblings tend nous inotropic (dopamine) or beta blockers (pro- to sufer from the same disease. Chromosomal defects, say Down syndrome, z Urinary output trisomy 13–15, trisomy 16–18, Turner syndrome, etc. Congenital aortic stenosis Atrial septal defect involving fossa ovalis (not fossa Vascular rings secundum) may close spontaneously. Ebstein anomaly Pulmonary arterial hypertension, polycythemia, Increased pulmonary blood fow hemiplegia, brain abscess, hypercyanotic (tet spells) z Transposition of the great arteries (right-to-left shunt). Recurrent respiratory infections, heart failure, arrhythmias, aortic regurgitation (left-to-right shunt). In the frst situation, parents need to be encouraged if Spontaneous Closure/Corrections they intend to have another child. As soon as ratio of pulmonary defects are in membranous portion of the interventricular to systemic vascular resistance approaches 1:1, the shunt septum; only 10% defects are in muscular septum. Te enlargement of the chambers depends on the shunts which further depend on the ratio of the pulmonary Hemodynamics/Pathophysiology to systemic blood fow. Te large volume of pulmonary blood fow causes 1 cm), pulmonary vascular resistance at birth is higher enlargement of the pulmonary artery trunk, left atrium and than normal. However, with the reduction in Clinical Features the resistance in the next few weeks, the shunt magnitude If septal defect is small, there may be no symptoms at all. Moderate: One-third to two-thirds of diameter of aorta Small: Less than one-third of diameter of aorta Diagnosis Pinhole: Less than 2 mm (detectable by color Doppler only). Minimal cardiomegaly and Single slight increase in pulmonary vascularity may be noticed Multiple: Swiss-cheese type. Ostium General measures include attention to good nutrition secundum defect (high in atrial septum) may be as large as 2 with treatment of iron defciency anemia and other nutri- cm. Heart failure and recurrent chest Rarely, it is associated with mitral stenosis infection are treated on usual lines. Yet, symptoms are absent or minimal in infants because the greater thickness and less resilience of muscular wall of the right ventricle limits the shunt. As the infant grows, the right ventricular wall becomes thin and more resilient, causing elevation in the shunt. Enlargement of the right atrium and ventricle and dilation of the pulmonary artery result from passage of large blood fow through the right heart. Nevertheless, pulmonary arterial pressure remains normal, pulmonary vascular resistance low and the left ventricle and aorta normal in size. In adulthood, when pulmonary vascular resistance begins to increase, cyanosis may occasionally Fig. Atrial septal defect remains asymptomatic in most of the z Increased ventricular end-diastolic dimension. Another z Localization of the exact size and position of atrial important feature is growth failure, which may be the only defect by real-time two-dimensional scans from manifestation in some children. Te typical murmur is ejection systolic, soft, and best Cardiac catheterization shows oxygen content of heard over upper left sternal border (usually the second blood from right atrium to be far more than that from intercostal space). Tese are infrequent, especially in infants: Diagnosis Heart failure seldom occurs in infancy Infective endocarditis is infrequent Chest X-ray shows right atrial and ventricular Pulmonary hypertension enlargement, increased pulmonary vascularity, enlarged Eisenmenger complex pulmonary artery and rather small left ventricle and aorta (Fig. Echocardiography shows evidence typical circulation without getting opportunity to be fltered of right ventricle overload, say: by the lungs as in a normal case. Te closure of defect by open heart surgery gives In case of a large shunt, a third heart sound followed by gratifying results. Patent ductus arteriosus, persistence of a communication between aorta and pulmonary artery, is unique in two Complications ways. Firstly, it occurs most often as an isolated defect Heart failure which is unlike most other congenital cardiac anomalies. Infective endocarditis Secondly, it occurs twice as frequently in girls as in boys. Pulmonary arterial hypertension Rarely, aneurysmal dilatation of pulmonary artery and/ Hemodynamics/Pathophysiology or ductus, calcifcation of ductus, thromboembolism, Te magnitude of the right-to-left shunt depends on Eisenmenger syndrome and rheumatic heart disease. Diagnosis Since pressure gradient in aorta is dominant, blood Radiology reveals biventricular enlargement, promi- fow is from aorta to pulmonary artery. In advanced cases, nent aortic knob and pulmonary artery and plethoric almost half or more of left ventricular output may be lungs with hilar dance (Fig. In extreme degree of disease, Electrocardiography is usually normal, but may show pulmonary hypertension may develop. Deep Q waves may be seen in such a patient may develop pulmonary vascular disease. Run of of blood into pulmonary artery during systole Echocardiogram is essentially normal in a small accounts for the high pulse pressure. In case of a large ductus, there is an increase in left atrial and ventricular dimensions and decrease in Clinical Features isovolumetric contraction time (Fig. Patent ductus arteriosus may become manifest with heart failure in second or third month of life. Symptomatic cases have growth retardation, recurrent respiratory infections, exertional dyspnea (efort intolerance), palpitations, and heart failure. Occasionally, precordial pain and hoarseness (due to recurrent laryngeal nerve involvement) may be present. Pulse pressure is wide because of leak of systemic blood from aorta to pulmonary artery. As a result, water- hammer pulse and prominent arterial Corrigan (carotid) pulsationsin the neck may be present. Diferential cyanosis, in which left arm and both feet are involved, may be observed. It begins immediately after the frst heart sound and reaches its peak at the end of systole. It continues in a reduced intensity during most of diastolic phase (though audible during a part of diastolic phase), gradually disappearing in the later part. It is harsh and best heard at the second left intercostal space away from the left sternal border (Gibson’s area) and transmitted to area below the left clavicle, and, at times, lower down, i. Pulmonary stenosis afects both the infundibulum and the pulmonary valve and artery. Infundibular stenosis is in part because of anterior deviation of the infundibular portion of the ventricular septum. Pulmonary stenosis is almost always present, though it is seldom the only site of obstruction. When the right ventricle contracts, it meets much resistance at the pulmonary stenosis. Te right-sided blood is, therefore, shunted through the ventricular defect into the left ventricle and then on to aorta. Te net result is persistent arterial unsaturation, polycythemia, cyanosis and poor pulmonary vascularity. Occasionally, the degree of obstruction is small and the right-to-left shunt is minimal or absent.