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### Samir rafla principles of cardiology pages 1 61

1. 1. Principles of Cardiology pages 1-61 ELECTROCARDIOGRAPHY Prof. Samir RaflaThe electrocardiogram (ECG) is a graphic representation of the electrical activitygenerated by the heart during the cardiac cycle. The electrical activity starts from theSA node, bundle of His, right and left bundles, Purkinje fibers to stimulate theventricles.Waveforms: The waveforms and intervals of the ECG are: The P wave = atrialdepolarization. The QRS complex = ventricular depolarization. The Q wave is theinitial downward deflection, the R wave is the initial upward deflection, and the Swave is the second downward deflection. The interval from the beginning of the Pwave to the beginning of the Q wave is the PR interval.The T wave = ventricular repolarization. The interval from the end of ventriculardepolarization to the beginning of the T wave is termed the ST segment. The intervalfrom the onset of ventricular depolarization to end of T is the QT interval.STANDARD APPROACH TO THE ECG: Normally, standardization is 1.0 mVper 10 mm, and paper speed is 25 mm/s (each horizontal small box = 0.04 sec)Heart Rate: divide 1500 by number of small boxes between each QRS.Rhythm: Sinus rhythm is present if every P wave is followed by a QRS, PR interval >0.12 s, and the P wave is upright in leads I, II, and III.Intervals: PR (0.12 - 0.20 s). QRS (0.06 - 0.10 s).QT 0.43 s;ST-T WAVES: ST elevation : Acute MI, coronary spasm, pericarditis (concaveupward), LV aneurysm.ST depression: Digitalis effect, strain (due to ventricular hypertrophy), ischemia, ornontransmural MI.Tall peaked T: Hyperkalemia; acute MI ("hyperacute T").Inverted T: Non-Q-wave MI, ventricular "strain" pattern, drug effect (e.g., digitalis),hypokalemia, hypocalcemia, increased intracranial pressure (e.g., subarachnoidbleeding).
2. 2. FIG: The magnified ECG wave is presented with the principal time intervals indicated. Fig: The pathways of Conduction. 2
3. 3. RHEUMATIC FEVERIntroduction. Classified as a connective tissue or collagen vascular disease,rheumatic fever (RF) is the leading cause of acquired heart disease in children andyoung adults.a. In many developing countries the incidence of acute RF approaches or exceeds 100per 100.000, whereas in the Unites States it is estimated to be less than 2 per 100.000.b. Rheumatic fever is more common among population at high risk for streptococcalpharyngitis, those in close contact with school age children, and persons of lowsocioeconomic status. It occurs commonly between the ages of 5 and 18 years and israre before 5. Rheumatic fever affects both sexes equally, except for Sydenham’schorea, which is more prevalent in females after puberty.The clinical manifestations of RF develop after a silent period of approximately 3weeks following a tonsillopharyngitis caused by a group A streptococcal infection(GAS).Diagnostic criteria1. The Jones criteria, are designed to aid in the diagnosis of the first episode ofRF. Rheumatic fever can be diagnosed when a previous upper airway infection withGA-Streptococci is detected in conjunction with either two major manifestations, orone major and two minor manifestations. Major manifestation includes arthritis,carditis, chorea, erythema marginatum, and subcutaneous nodules.Minor manifestations include: fever, arthralgias, history of tonsillitis 1-3 weeks beforethe arthralgia, history of rheumatic heart disease;high C-reactive protein, high erythrocyte sedimentation rate, raised antistreptolysin Otiter above 200 Todd’s units or prolonged PR interval on electrocardiogram (ECG).Major manifestations:1. Carditis: affecting 41% to 83% of patients. It can be defined as pancarditis affectingthe endocardium, myocardium, and pericardium: The main clinical manifestationsinclude increased heart rate, murmurs, cardiomegaly, rhythm disturbances, pericardialfriction rub, and heart failure. Congestive heart failure is rare in the acute phase; ifpresent, it usually results from myocarditis. The most characteristic component ofrheumatic carditis is a valvulitis (endocarditis) involving the mitral and aortic valves.Pericarditis may cause chest pain, friction rubs, and distant heart sounds. 3
4. 4. 2. Arthritis. This is the most common manifestation of RF. It is present in around80% of the patients and has been described as painful, asymmetric, migratory, andtransient; it involves large joints, such as knees, ankles, elbows, wrists, and shoulders.It improves markedly with the use of salicylates within 48 hours of treatment.Monoarthritis, oligoarthritis, and involvement of small joints of the extremities areless common. The arthritis of RF is benign and self- limiting (Lasting 2 to 3 weeks)and does not result in permanent sequelae.3. Sydenham’s chorea. This extrapyramidal disorder is characterized by purposelessand involuntary movements of face and limbs, muscular hypotonia, and emotionallability.4. Subcutaneous nodules.5. Erythema marginatum.Minor manifestations:1. Fever is encountered during the acute phase of the disease.2. Arthralgia is defined as pain in one or more large joints without objective findingsof inflammation on physical examination.3. Other clinical manifestations of RF include abdominal pain, epistaxis, acuteglomerulonephritis. These are not included as diagnostic criteria for the diagnosis ofRF.Laboratory examination and diagnostic testing.1. Neither throat culture nor rapid antigen test, if positive; differentiatebetween recent infection associated with RF and chronic carriage ofpharyngeal GAS.2. Antistreptolysin O is the most commonly available test. Elevated or rising ASOtiters provide solid evidence for recent GAS infection. A greater than two-fold rise inASO titers compared with convalescent titers is diagnostic.3. Increased sedimentation rate.4. Increased C reactive protein CRP/5. The most common finding in the electrocardiogram is the presence of P-Rprolongation and sinus tachycardia. 4
5. 5. Therapy:Patient with the diagnosis of rheumatic activity should initially receive a full course ofantibiotic to ensure proper eradication of the organism.A. Arthritis: Anti-inflammatory medications are generally recommended for 3 weeksfor symptomatic relief.1. Pain resolves within 24 hours of starting therapy with salicylates.2. If pain persists after salicylate treatment, the diagnosis of RF is questionable.3. The recommended dose of salicylate is 100 mg/kg per day, given in 4 divideddoses. Toxic effects such as anorexia, nausea, vomiting, and tinnitus should beavoided.B. Carditis1. Strenuous physical activity should be avoided.2. Congestive heart failure should be treated with appropriate therapy.3. In patients with significant cardiac involvement, corticosteroids are preferred oversalicylates. The recommended dose is 1 to 2 mg/kg per day, (maximum of 60 mg/dayas Prednisolone). Commonly, therapy is needed for more than one month in patientswith cardiac involvement. Therapy should be continued until there is sufficientclinical and laboratory evidence of disease inactivity.4. The gradual reduction in steroid doses is important to avoid relapses. Use ofsalicylates (75 mg/kg per day) while tapering corticosteroids may reduce thelikelihood a relapse. Summary: Jones Criteria of Rheumatic FeverMajor Criteria Minor CriteriaMigratory polyarthritis FeverCarditis ArthralgiaChorea High sedimentation rateSubcutaneous nodules Positive C reactive proteinErythema Marginatum Prolonged PR intervalPrevention:The most important step in the treatment of RF is the eradication of GAS infection. 5
6. 6. Penicillin is the agent of choice. A. best results are achieved with a singleintramuscular dose of penicillin G benzathine. b. The oral antibiotic of choice ispenicillin V (phenoxymethyl penicillin) (see Table for dosage information). Patientsallergic to penicillin: oral erythromycin can be used. The recommended dosage iserythromycin for 10 days. The maximal dose of erythromycin is 1 g/day.Table: Duration of therapy for secondary prevention of rheumatic fever Disease state Duration of therapy RF + carditis + residual valvular At least 10 years post episode and at least disease until age 40. Lifelong prophylaxis may be required RF + carditis without valvular 10 years or beyond adulthood, whichever disease is longer. RF without carditis 5 years or until age of 21, whichever is longer. RF, rheumatic fever. VALVULAR HEART DISEASE MITRAL STENOSISETIOLOGY AND PATHOLOGY: Two-thirds of all patients with mitral stenosis(MS) are females. MS is generally rheumatic in origin. Pure or predominant MSoccurs in approximately 40% of all patients with rheumatic heart disease. The valveleaflets are diffusely thickened by fibrous tissue and/or calcific deposits. The mitralcommissures fuse, the chordae tendineae fuse and shorten. The valvular cusps becomerigid, and these changes in turn, lead to narrowing at the apex of the funnel-shapedvalve.Other rare causes of mitral stenosis: Atrial myxoma, ball valve thrombus, congenitaland calcific-atherosclerortic disease.PATHOPHYSIOLOGY: In normal adults the mitral valve orifice is 4 to 6 cm 2. Whenthe mitral valve opening is reduced to 1 cm2, a left atrial pressure of approximately 25mmHg is required to maintain a normal cardiac output. The elevated left atrial 6
7. 7. pressure, in turn, raises pulmonary venous and capillary pressures, reducingpulmonary compliance and causing exertional dyspnea.Pulmonary hypertension results from (1) the passive backward transmission of theelevated left atrial pressure, (2) pulmonary arteriolar constriction, (reactive pulmonaryhypertension), and (3) organic obliterative changes in the pulmonary vascular bed. Intime, the resultant severe pulmonary hypertension results in tricuspid and pulmonaryincompetence as well as right-sided heart failure.SYMPTOMS AND COMPLICATIONS: - Dyspnea, hemoptysis. - Orthopnea andparoxysmal nocturnal dyspnea. Pulmonary edema develops when there is a suddensurge in flow across a markedly narrowed mitral orifice.The cardiac cycle: Simultaneous electrocardiogram and pressure obtained from theleft atrium, left ventricle, and aorta, and the jugular pulse during one cardiac cycle. 7
8. 8. When moderately severe MS has existed for several years, atrial arrhythmias as flutterand fibrillation occur.Hemoptysis results from rupture of pulmonary-bronchial venous connections(apoplexy) secondary to pulmonary venous hypertension. Frank hemoptysis must bedistinguished from the bloody sputum that occurs with pulmonary edema, pulmonaryinfarction, and bronchitis, three conditions that occur with increased frequency in thepresence of MS.Recurrent pulmonary emboli, sometimes with infarction are an important cause ofmorbidity and mortality late in the course of MS, occurring most frequently inpatients with right ventricular failure. Pulmonary infections, i.e., bronchitis, broncho-pneumonia, and lobar pneumonia, commonly complicate untreated MS. Infectiveendocarditis is rare in pure MS but is not uncommon in patients with combinedstenosis and regurgitation.Summary: Causes of hemoptysis in mitral stenosis:- Bronchitis- Congestion- Pulmonary edema- Pulmonary embolism, infarction- Pulmonary apoplexyThrombi and emboli: Thrombi may form in the left atrium, particularly in theenlarged atrial appendage of patients with MS. If they embolize, they do so mostcommonly to the brain, kidneys, spleen, and extremities. Embolization occurs muchmore frequently in patients with atrial fibrillation. Rarely, a large pedunculatedthrombus or a free-floating clot may suddenly obstruct the stenotic mitral orifice.Such “ball valve” thrombi produce syncope, angina, and changing auscultatory signswith alterations in position, findings that resemble those produced by a left atrialmyxoma.PHYSICAL FINDINGS: Inspection: In advanced cases there is a malar flush. Whenfibrillation is present, the jugular pulse reveals only a single expansion during systole(c-v wave) (systolic venous pulse). 8
9. 9. Palpation: Left parasternal lift along the left sternal border signifies an enlarged rightventricle. In patients with pulmonary hypertension, the impact of pulmonary valveclosure can usually be felt in the second and third left intercostal spaces just left of thesternum (Diastolic shock). A diastolic thrill is frequently present at the cardiac apex,particularly if the patient is turned into the left lateral position.Auscultation: The first heart sound (S1) is generally accentuated and snapping. Inpatients with pulmonary hypertension, the pulmonary component of the second heartsound (P2) is often accentuated, and the two components of the second heart sound areclosely split. The opening snap (OS) of the mitral valve is most readily audible inexpiration at, or just medial to, the cardiac apex but also may be easily heard along theleft sternal edge. This sound generally follows the sound of aortic valve closure (A2)by 0.05 to 0.12; that is, it follows P2; the time interval between A2 closure and OSvaries inversely with the severity of the MS. It tends to be short (0.05 to 0.07 s) inpatients with severe obstruction, and long, (0.10 to 0.12 s) in patients with mild MS.The intensities of the OS and S1 correlate with mobility of the anterior mitral leaflet.The OS usually precedes a low-pitched, rumbling, diastolic murmur, heard best at theapex with the patient in the left lateral recumbent position. In general, the duration ofthe murmur correlates with the severity of the stenosis. In patients with sinus rhythm,murmur often reappears or becomes accentuated during atrial systole, as atrialcontraction elevates the rate of blood flow across the narrowed orifice (presystolicaccentuation). Associated lesion: With severe pulmonary hypertension, a pansystolic murmurproduced by functional tricuspid regurgitation may be audible along the left sternalborder. Characteristically, this murmur is accentuated by inspiration, and should notbe confused with the apical pansystolic murmur of mitral regurgitation. In the presence of severe pulmonary hypertension and right ventricular failure, athird heart sound may originate from the right ventricle. The enlarged right ventriclemay rotate the heart in a clockwise direction and form the cardiac apex, giving theexaminer the erroneous impression of left ventricular enlargement. Under thesecircumstances, the rumbling diastolic murmur and the other auscultatory features ofMS become less prominent or may even disappear and be replaced by the systolic 9
10. 10. murmur of functional tricuspid regurgitation which is mistaken for mitralregurgitation. When cardiac output is markedly reduced in a patient with MS, thetypical auscultatory findings, including the diastolic rumbling murmur, may not bedetectable (silent MS).ECG findings: The P wave is wide and may be notched which suggests left atrialenlargement. It becomes tall and peaked in lead II and upright in lead V1 when severepulmonary hypertension. 10
11. 11. Echocardiogram: Two-dimensional echo-Doppler echocardiography for estimationof the transvalvular gradient and of mitral orifice size, the presence and severity ofaccompanying mitral regurgitation, the extent of restriction of valve leaflets, theirthickness, and the subvalvular changes. Transthoracic and transesophageal echo areneeded to verify presence of atrial thrombi.X-Ray chest: Straightening of the left border of the cardiac silhouette, prominence ofthe main pulmonary arteries, dilatation of the upper lobe pulmonary veins, andbackward displacement of the esophagus by an enlarged left atrium. Summary of signs of mitral stenosis:- Mid-diastolic rumbling murmur with presystolic accentuation;- Snappy first sound;- Opening snap;- Diastolic thrill.DIFFERENTIAL DIAGNOSIS: The apical middiastolic murmur associated withaortic regurgitation (Austin Flint murmur) may be mistaken for MS. However, in apatient with aortic regurgitation, the absence of an opening snap or presystolicaccentuation if sinus rhythm is present points to the absence of MS.Tricuspid stenosis, a valvular lesion that occurs very rarely in the absence of MS, maymask many of the clinical features of MS.MANAGEMENT: Penicillin prophylaxis of beta-hemolytic streptococcal infectionsand prophylaxis for infective endocarditis are important. In symptomatic patients,some improvement usually occurs with restriction of sodium intake and maintenancedoses of oral diuretics. Digitalis glycosides usually do not benefit patients with purestenosis and sinus rhythm, but they are necessary for slowing the ventricular rate ofpatients with atrial fibrillation and for reducing the manifestations of right-sided heartfailure in the advanced stages of the disease. 11
12. 12. Small doses of beta-blockers (e.g., atenolol 25 mg/d) may be added when cardiacglycosides fail to control ventricular rate in patients with atrial fibrillation. Particularattention should be directed toward detecting and treating any accompanying anemiaand infections. Hemoptysis is treated by measures designed to diminish pulmonaryvenous pressure, including bed rest, the sitting position, salt restriction, and diuresis.Anticoagulants should be administered continuously in those with atrial fibrillation.If atrial fibrillation is of relatively recent origin in a patient who’s MS is not severeenough to warrant surgical treatment, reversion to sinus rhythm pharmacologically orby means of electrical countershock is indicated. Usually this should be undertakenfollowing 3 weeks of anticoagulant treatment. Conversion to sinus rhythm is rarelyhelpful in patients with severe MS, particularly those in whom the left atrium isespecially enlarged or in whom atrial fibrillation is chronic.Mitral valvotomy by balloon or surgical mitral valvotomy, is indicated in thesymptomatic patient with pure MS whose effective orifice is less than approximately1.3 cm2 (or 0.8 cm2 / m2 of body surface area). Mitral valve replacement by prostheticvalve is resorted to only if the valve is heavily calcified and associated withincompetence.Percutaneous balloon valvuloplasty is an alternative to surgical mitral valvuloplasty inpatients with pure or predominant rheumatic stenosis (it is now the first choice).Young patients without extensive valvular calcification or thickening or subvalvulardeformity are the best candidates for this procedure.Contraindications of balloon mitral valvotomy:1. presence of left atrial thrombi,2. presence of combined mitral incompetence and stenosis, and3. heavily calcified mitral cusps. 12
13. 13. MITRAL REGURGITATIONETIOLOGY:1- Chronic rheumatic heart disease is the cause of severe mitral regurgitation (MR).2- MR also may occur as a congenital anomaly.3- MR may occur in patients with infarction involving the base of a papillarymuscle.4- MR may occur with marked left ventricular dilatation.5- Massive calcification of the mitral annulus of unknown cause, presumablydegenerative, which occurs most commonly in elderly women.6- Systemic lupus erythematosus, rheumatoid arthritis, are less common cause.7- Mitral prolapse.Acute MR occur 1- secondary to infective endocarditis involving the cusps orchordae tendineae, 2- in acute myocardial infarction with rupture of a papillarymuscle or one of its heads, 3- as a consequence of trauma, 4- or following apparentlyspontaneous chordal rupture.MITRAL REGURGITATION: SYMPTOMS: Fatigue, exertional dyspnea, andorthopnea are the most prominent complaints in patients with chronic, severe MR.Hemoptysis and systemic embolism also occur less frequently in MR than in MS.Right-sided heart failure, with painful hepatic congestion, ankle edema, distendedneck veins, ascites, and tricuspid regurgitation, may be observed in patients with MRwho have associated pulmonary vascular disease and marked pulmonaryhypertension. In patients with acute, severe MR, left ventricular failure with acutepulmonary edema and /or cardiovascular collapse is common.PHYSICAL FINDINGS: Palpation: A systolic thrill is often palpable at the cardiacapex, the left ventricle is hyperdynamic, and the apex beat is often displaced laterally.Auscultation: The first heart sound is generally absent, soft (muffled), or buried in thesystolic murmur. A low-pitched third heart sound (S3) occurring 0.12 to 0.17 sec afteraortic valve closure, i.e. at the completion of the rapid-filling phase of the leftventricle, is an important auscultatory feature of severe MR. 13
14. 14. A fourth heart sound is often audible in patients with acute, severe MR of recent onsetwho are in sinus rhythm. A systolic murmur of at least grade III/VI intensity is themost characteristic auscultatory finding in severe MR. It is usually holosystolic(pansystolic). In MR due to papillary muscle dysfunction or mitral valve prolapse, thesystolic murmur commences in midsystole. In patients with ruptured chordaetendineae the systolic murmur may have a cooing or “sea gull” quality; in patientswith a flail leaflet the murmur may have a musical quality. Summary: Signs of mitral incompetence:- Harsh pansystolic murmur over apex propagated to axilla.- Muffled first heart sound.- Systolic thrill over apex.Electrocardiogram: In patients with sinus rhythm there is evidence of left atrialenlargement (P mitrale), but right atrial enlargement also may be present whenpulmonary hypertension is severe. Chronic, severe MR with left atrial enlargement isgenerally associated with atrial fibrillation.Echocardiogram: Doppler echocardiography and color Doppler flowechocardiography imaging are the most accurate noninvasive techniques for thedetection and estimation of MR. The left atrium is usually enlarged. Findings whichhelp to determine the etiology of MR can often be identified; these includevegetations associated with infective endocarditis, incomplete coaptation of theanterior and posterior mitral leaflets, and annular calcification, as well as leftventricular dilation, aneurysm, or dyskinesia. The echocardiogram in patients withmitral valve prolapse is described below.Roentgenogram: The left atrium and left ventricle are the dominant chambers; inchronic cases, the former may be massively enlarged and forms the right border of thecardiac silhouette. Pulmonary venous congestion, interstitial edema, and Kerly B linesare sometimes noted.TREATMENT: Medical: The non surgical management of MR is directed towardrestricting those physical activities that regularly produce dyspnea and excessivefatigue, reducing sodium intake, and enhancing sodium excretion with the appropriate 14
15. 15. use of diuretics. Vasodilators and digitalis glycosides increase the forward output ofthe failing left ventricle. Angiotensin-converting enzyme inhibitors are given inchronic MR. The same considerations as in patients with MS apply to the reversion ofatrial fibrillation to sinus rhythm. Surgical treatment should be offered to patients withsevere MR whose limitations do not allow them to perform normal householdactivities despite optimal medical management. Surgery is indicated when the endsystolic diameter of the left ventricle by echo exceeds 50 mm. MITRAL VALVE PROLAPSEMitral valve prolapse (MVP), also termed the systolic click-murmur syndrome, is acommon, but highly variable, clinical syndrome. It is a frequent finding in patientswho have the typical features of the Marfan syndrome. The posterior leaflet is usuallymore affected than the anterior, and the mitral valve annulus is often greatly dilated.MVP may be associated with thoracic skeletal deformities.MVP is common in females between the ages of 6 and 30 years. Most patients areasymptomatic and remain so for their entire lives. Arrhythmia, most commonlyventricular premature contractions and paroxysmal supraventricular and ventriculartachycardia, have been reported and may cause palpitations, light-headedness, andsyncope. Many patients have chest pain which is difficult to evaluate.PHYSICAL EXAMINATION: Auscultation: the most important finding is the mid-orlate (nonejection) systolic click, which occurs 0.14 s or more after the first heartsound. Systolic clicks may be followed by a high-pitched late systolic murmur, heardbest at the apex. A useful echocardiographic definition of MVP is systolicdisplacement (in the parasternal view) of the mitral valve leaflets into the left atrium >3 mm. Thickening of the mitral valve leaflets is present. Doppler studies are helpful inrevealing and evaluating accompanying MR.Treatment: The management of patients with MVP consists of reassurance of theasymptomatic patient without severe MR or arrhythmias; prevention of infectiveendocarditis with antibiotic prophylaxis in patients with a systolic murmur and therelief of the atypical chest pain by beta blockers. 15
16. 16. AORTIC STENOSISAortic stenosis (AS) occurs in one-fourth of all patients with chronic valvular heartdisease; approximately 80 percent of adult patients with symptomatic valvular AS aremale.Etiology: 1. AS may be congenital in origin, 2. secondary to rheumatic inflammationof the valve, 3. degenerative calcification of the aortic cusps of unknown cause.PATHOPHYSIOLOGY: A peak systolic pressure gradient exceeding 50 mmHg or aneffective aortic orifice less than approximately 0.5 cm2/m2 of body surface area i.e.,less than approximately one-third of the normal orifice, is generally considered torepresent critical obstruction to left ventricular outflow.SYMPTOMS: AS is rarely of hemodynamic or clinical importance until the valveorifice has narrowed to approximately one-third of normal, i.e., to 1 cm2 in adults.Exertional dyspnea, angina pectoris, and syncope are the three cardinal symptoms.Angina pectoris reflects an imbalance between the augmented myocardial oxygenrequirement by the hypertrophied myocardium and the un-accompanying increase incoronary blood flow. Orthopnea, paroxysmal nocturnal dyspnea, and pulmonaryedema, i.e., symptoms of left ventricular failure, also occur only in the advancedstages of the disease.PHYSICAL FINDINGS: A palpable double systolic arterial pulse the so-calledbisferiens pulse, excludes pure or predominant AS and signifies dominant or pureaortic regurgitation or obstructive hypertrophic cardiomyopathy.Palpation: The apex beat is usually sustained and displaced laterally, reflecting thepresence of left ventricular hypertrophy. A systolic thrill is generally present at thebase of the heart in the suprasternal notch, and along the carotid arteries.Auscultation: Harsh ejection systolic murmur over aortic area propagated to carotids.The sound of aortic valve closure, the second sound is very weak or even absent withtight aortic stenosis. Frequently, a fourth heart sound is audible at the apex in many patients withsevere AS and reflects the presence of left ventricular hypertrophy and an elevatedleft ventricular enddiastolic pressure; a third heart sound generally occurs when theleft ventricle dilates and fails. 16
17. 17. The murmur of AS is characteristically an ejection systolic murmur loudest at thebase of the heart, most commonly in the second right intercostal space. It istransmitted along the carotid arteries. Occasionally, it is transmitted downward and tothe apex and may be confused with the systolic murmur of MR. Summary: Signs of aortic stenosis:1. Harsh ejection systolic murmur over aortic area propagated to carotids.2. Weak or absent second heart sound (aortic component)3. Systolic thrill over aortic area, suprasternal notch and carotids.4. Strong sustained apex,Electrocardiogram: This reveals left ventricular hypertrophy in the majority ofpatients with severs AS.Echocardiogram: The key findings are left ventricular hypertrophy. The transaorticvalvular gradient can be estimated by Doppler echocardiography.Congestive heart failure was considered to be the cause of death in one-half to two-thirds of patients. Among adults dying with valvular AS sudden death, whichpresumably results from an arrhythmia (ventricular tachycardia or fibrillation)occurred in 10 to 20 percent and at an average age of 60 years.TREATMENT: All patients with moderate or severe AS require careful periodicfollow-up. In patients with severe AS, strenuous physical activity should be avoidedeven in the asymptomatic stage. Digitalis glycosides, sodium restriction, and thecautious administration of diuretics are indicated in the treatment of congestive heartfailure, but care must be taken to avoid volume depletion.In the majority of adults with calcific AS and critical obstruction, replacement of thevalve is necessary. Percutaneous balloon aortic valvuloplasty is an alternative tosurgery in children and young adults with congenital aortic stenosis. It is notcommonly employed in elderly with severe calcific aortic stenosis because of a highrestenosis rate. 17
18. 18. Electrocardiogram (ECG), left ventricular, and aortic pressure curves in a patient withaortic stenosis. There is a pressure gradient across the aortic valve during systoleFig. Abnormal sounds and murmurs associated with valvular dysfunction displayedsimultaneously with left atrial (LA), left ventricular (LV), and aortic pressure tracings.AVO, aortic valve opening; E, ejection click; MVO, mitral valve opening; OS,opening snap of the mitral valve.. 18
19. 19. AORTIC REGURGITATIONETIOLOGY: Approximately three-fourths of patients with pure or predominant aorticregurgitation (AR) are males; females predominate among patients with AR who haveassociated mitral valve disease.Causes:1- In approximately two-thirds of patients with AR the disease is rheumatic in origin,resulting in thickening, deformation and shortening of the individual aortic valvecusps, changes which prevent their proper opening during systole and closure duringdiastole.2- Acute AR also may result from infective endocarditis, which may attack a valvepreviously affected by rheumatic disease, a congenitally deformed valve, or rarely anormal aortic valve, and perforate or erode one or more of the leaflets.3- Patients with discrete membranous subaortic stenosis often develop thickening ofthe aortic valve leaflets, which in turn leads to mild or moderate degrees of AR.4- AR also may occur in patients with congenital bicuspid aortic valves.5- Aortic dilatation, i.e., aortic root disease, widening of the aortic annulus andseparation of the aortic leaflets are responsible for the AR.6- Syphilis and ankylosing rheumatoid spondylitis may lead to aortic dilatation,aneurysm formation, and severe regurgitation.7- Cystic medial necrosis of the ascending aorta, associated with other manifestationsof the Marfan syndrome, idiopathic dilatation of the aorta, and severe hypertension allmay widen the aortic annulus and lead to progressive AR.8- Occasionally, AR is caused by retrograde dissection of the aorta involving theaortic annulus.History: Patients with severe AR may remain asymptomatic for 10 to 15 years.Sinus tachycardia during exertion may produce particularly uncomfortablepalpitations. Exertional dyspnea is the first symptom of diminished cardiac reserve.This is followed by orthopnea, paroxysmal nocturnal dyspnea, and excessivediaphoresis. Chest pain occurs frequently, even in younger patients, due to diminishedcoronary filling during diastole. 19
20. 20. Nocturnal angina may be a particularly troublesome symptom. The anginal episodescan be prolonged and often do not respond satisfactorily to sublingual nitroglycerin.Late in the course of the disease, evidence of systemic fluid accumulation, includingcongestive hepatomegaly, ankle edema, and ascites, may develop.PHYSICAL FINDINGS: Peripheral signs: Arterial pulse: A rapidly rising “water-hammer” pulse, which collapses suddenly as arterial pressure falls rapidly during latesystole and diastole, and capillary pulsations, an alternate flushing and paling of theroot of the nail while pressure is applied to the tip of nail, are characteristic of freeAR. A booming, “pistol-shot” sound can be heard over the femoral or brachialarteries, and a to - fro murmur is audible if the femoral artery is lightly compressedwith a stethoscope.The arterial pulse pressure is widened, with an elevation of the systolic pressure and adepression of the diastolic pressure. The severity of AR does not always correlatedirectly with the arterial pulse pressure, and severe regurgitation may exist in patientswith arterial pressures in the range of 140/60.Palpation: The apex beat is strong and displaced laterally and inferiorly. The systolicexpansion and diastolic retraction of the apex are prominent and contrast sharply withthe sustained systolic thrust characteristic of severe AS. In many patients with pureAR or with combined AS and AR, palpation or recording of the carotid arterial pulsereveals it to be bisferiens, i.e., with two systolic waves separated by trough.Auscultation: A third heart sound is common, and occasionally, a fourth heart soundalso may be heard. The murmur of AR is typically a high-pitched, blowing,decrescendo early diastolic murmur which is usually heard best in the third leftintercostal space. Unless it is trivial in magnitude, the AR is usually accompanied byperipheral signs such as a widened pulse pressure or a collapsing pulse. On the otherhand, with the Graham steel murmur of pulmonary regurgitation, there is usuallyclinical evidence of severe pulmonary hypertension, including a loud and palpablepulmonary component to the second heart sound. A midsystolic ejection murmur is frequently audible in AR. It is generally heardbest at the base of the heart and is transmitted to the carotid vessels. This murmur may 20
21. 21. be quite loud without signifying organic obstruction; it is often higher pitched,shorter, than the ejection systolic murmur heard in patients with predominant AS. A third murmur which is frequently heard in patients with AR is the Austin Flintmurmur, a soft, low-pitched, rumbling middiastolic or presystolic bruit. It is probablyproduced by the displacement of the anterior leaflet of the mitral valve by the aorticregurgitant stream. Both the Austin Flint murmur and the rumbling diastolic murmurof MS are loudest at the apex, but the murmur of MS is usually accompanied by aloud first heart sound and immediately follows the opening snap of the mitral valve,while the Austin Flint murmur is often shorter in duration than the murmur of MS,and in patients with sinus rhythm the latter exhibits presystolic accentuation. Summary: Signs of aortic incompetence over the heart:- Soft blowing early diastolic murmur over aortic area propagated to apex.- Austin-Flint murmur (diastolic murmur over mitral area).Echocardiogram: Essential for detection of severity and cause of AR.TREATMENT: Although operation constitutes the principal treatment of aorticregurgitation, and should be carried out before the development of heart failure, thelatter usually respond initially to treatment with digitalis, salt restriction, diuretics, andvasodilators, especially angiotensin-converting enzyme inhibitors.In patients with severe AR, careful clinical follow-up and noninvasive testing withechocardiography at approximately 6-month intervals are necessary. Operation is tobe undertaken at the optimal time, i.e., after the onset of left ventricular dysfunctionbut prior to the development of severe symptoms. Valve replacement is indicated ifthe LV dilates to 50 mm in systole and 65 to 70 mm in diastole.ACUTE AORTIC REGURGITATION: Infective endocarditis, aortic dissection, andtrauma are the most common causes of severe, acute AR. TRICUSPID STENOSISIt is generally rheumatic in origin and is more common in women than in men. It doesnot usually occur as an isolated lesion or in patients with pure MR but is usually 21
22. 22. observed in association with MS. Hemodynamically significant TS occurs in 5 to 10percent of patients with severe MS; rheumatic TS is commonly associated with somedegree of regurgitation.SYMPTOMS: Since the development of MS generally precedes that of TS, manypatients initially have symptoms of pulmonary congestion. Amelioration of the lattershould raise the possibility that TS may be developing. Fatigue secondary to a lowcardiac output and discomfort due to refractory edema, ascites, and markedhepatomegaly are common in patients with TS and / or regurgitation. Severe TS is associated with marked hepatic congestion, often resulting incirrhosis, jaundice, serious malnutrition, anasarca, and ascites. The jugular veins aredistended, and in patients with sinus rhythm there may be giant “a” waves.On auscultation, the pulmonic closure sound is not accentuated, and occasionally, anOS of the tricuspid valve may be heard approximately 0.06 s after pulmonic valveclosure. The diastolic murmur of TS has many of the quality of the diastolic murmurof MS, and since TS almost always occurs in the presence of MS, the less commonvalvular lesion may be missed. The murmur is augmented during inspiration, and it isreduced during expiration. Surgical treatment of the tricuspid valve is not ordinarily indicated at the time ofmitral valve surgery in patients with mild TS. On the other hand, definitive surgicalrelief of the TS should be carried out, preferable a the time of mitral valvotomy, inpatients with moderate or severe TS who have mean diastolic pressure gradientsexceeding 4 to 5 mmHg and tricuspid orifices less than 1.5 to 2.0 cm2. TS is almostalways accompanied by significant tricuspid regurgitation. TRICUSPID REGURITATION Most commonly, tricuspid regurgitation (TR) is functional and secondary tomarked dilatation of the right ventricle and the tricuspid annulus. Functional TR maycomplicate right ventricular enlargement of any cause, including inferior wall infarctsthat involve the right ventricle, and is commonly seen in the late stages of heart failuredue to rheumatic or congenital heart disease with severe pulmonary hypertension, aswell as in ischemic heart disease, cardiomyopathy, and cor pulmonale. It is in partreversible if pulmonary hypertension is relieved. Rheumatic fever may produce 22
23. 23. organic TR, often associated with TS. Endomyocardial fibrosis, infective endocarditismay produce TR. The clinical features of TR result primarily from systemic venous congestion andreduction of cardiac output. The neck veins are distended with prominent V waves,and marked hepatomegaly, ascites, pleural effusions, edema, systolic pulsations of theliver and positive hepato-jugular reflux are common. A prominent right ventricularpulsation along the let parasternal region and a blowing holosystolic murmur alongthe lower left sternal margin which may be intensified during inspiration and reducedduring expiration or the Valsalva maneuver are characteristic findings; AF is usuallypresent. Summary: Signs of tricuspid regurgitation- Pansystolic murmur over tricuspid area increases with inspiration.- Systolic neck vein pulsationsEchocardiography and Doppler: for detection of severity of TR, estimation ofpulmonary pressure and search for vegetations of infective endocarditis.Treatment of the underlying cause of heart failure usually reduces the severity offunctional TR. In patients with mitral valve disease and TR due to pulmonaryhypertension and massive RV enlargement, effective surgical correction of the mitralvalve abnormality results in lowering of the pulmonary vascular pressure and gradualreduction or disappearance of the TR. Tricuspid valvuloplasy by De Vega procedureand Carpentier ring can be done.Pulmonary Stenosis: See congenital pulmonary stenosisPulmonary RegurgitationDilatation of the pulmonary artery in cases of pulmonary hypertension may producepulmonary regurgitation. This is called Graham Steel murmur. It is differentiatedfrom the early diastolic murmur of aortic regurgitation by the associated signs ofpulmonary hypertension, and by Doppler study. 23
24. 24. CONGENITAL HEART DISEASECongenital heart malformations remain one of the most frequent birth defects, with alive-born prevalence of about 8 per 1000 live-born infants in western countries.Etiology of congenital heart disease: It is generally an abnormal form of cardiac development in the first 6-8 weeks ofintrauterine life. It is either due to exposure of the fetus in this period to injuriousteratogenic factor or to abnormal chromosomal structure.Some causes could be identified as:1- Drugs e.g. thalidomide, excess alcohol intake, anticonvulsant drugs.2- Exposure to radiation e.g. X-rays and gamma rays.3- Hereditary diseases: Diseases caused by chromosomal abnormalities eg Turnersyndrome, Down syndrome or mongolism.4- Maternal infections e.g. German measles in the first trimester of pregnancy. Congenital heart diseases in the adults could be classified into:I- Left or right ventricular outflow obstruction: Aortic stenosis, pulmonary stenosis,coarctation of aorta.II- Left to right shunts: ASD, VSD and PDA.III- Cyanotic heart disease: Fallot’s tetralogy and other cyanotic congenital diseases. LEET TO RIGHT SHUNTWhen there is a congenital communication between both sides of the heart, e.g. atrialor ventricular septal defects or patent ductus arteriosus the blood always flows fromthe left side (left atrium, left ventricle or aorta) to right side (right atrium, rightventricle or pulmonary artery). This is because the pressure in all left-sided chambersis higher than in right-sided chambers.EFFECTS:1- Left to right shunt results in pulmonary plethora (increased vascularity in the lung).If the shunt is very big heart failure may occur but this is rare.2- In mild to moderate cases the pulmonary vessels dilate to accommodate theexcessive blood flow. Mild cases are well tolerated but if the shunt is excessive the 24
25. 25. pulmonary vessels react by vasoconstriction. Pulmonary arteriolar vasoconstrictioncauses pulmonary hypertension which results in right ventricular hypertrophy.3- Pulmonary hypertension causes rise of pressure in the chambers of the right side ofheart. Ultimately the pressure in the right side exceeds that of the left side and theblood starts to flow across the defect in the reverse direction, i.e. right to left shunt(reversed shunt). The patient becomes cyanosed. Emboli originating in the venousside may be shunted across the defect to the arterial side and settle in organs such asthe brain or limbs. This is paradoxical embolism.Closure of the defect at this stage is useless and dangerous. This situation of acongenital defect + reversed shunt is called Eisenmenger’s syndrome. Eisenmenger’ssyndrome is not an independent congenital heart disease. It is the end result of big leftto right shunt. At this stage the clinical picture is that of central cyanosis with severepulmonary hypertension. ATRIAL SEPTAL DEFECTIn the presence of a defect in the atrial septum the right atrium receives blood bothfrom the normal venous return and the left atrium, the right atrium dilates. Thisresults in: Dilatation and hypertrophy of the right ventricle (volume overload),dilatation of the pulmonary artery, and pulmonary plethora. If the defect is big anduncorrected pulmonary arteriolar vasoconstriction progressively occurs and results inpulmonary hypertension usually at age 20-30 years. When the pressure in the rightatrium exceeds that in the atrium the shunt becomes reversed (Eisenmenger’ssyndrome) and the patient becomes cyanosed.Clinical features:1- Atrial septal defect is more common in females. When the left to right shunt is verybig pulmonary plethora may predispose to repeated chest infections in infancy.Otherwise there are no symptoms for many years. Ultimately heart failure occurs.2- Atrial fibrillation occurs in late cases.3- Right ventricular dilatation and hypertrophy cause a hyperdynamic impulse in thethird and fourth spaces to the left of the sternum and precordial bulge.4- Excessive flow across the tricuspid valve may produce a third heart sound andshort mid-diastolic murmur at the tricuspid area. 25
26. 26. 5- Excessive blood flow at the pulmonary valve may produce pulsations, dullness andan ejection systolic murmur in the pulmonary area.6- The specific auscultatory sign of atrial septal defect is wide fixed splitting of thesecond heart at the pulmonary area. The pulmonary component of the second sound isdelayed because the right ventricle takes a long time o empty the excessive volume ofblood it receives. The splitting dose not vary with respiration because: althoughinspiration causes increase in venous return, yet the resulting rise in right a trialpressure causes proportionate decrease in the left to right shunt so that the rightventricular output is constant and the time relation between aortic and pulmonarycomponents of the second sound remains constant.7- Progressive pulmonary hypertension occurs in big defects and result inEisenmenger syndrome. At this stage the clinical picture consists of: Central cyanosis,signs of pulmonary hypertension, and signs or right ventricular hypertrophy.X-RAY PICTURE:1- Plethoric lung fields. 2- Dilatation of the right atrium, right ventricle andpulmonary artery. 3- Marked pulsation of the pulmonary artery and its branches seenduring screening (hilar dance).ELECTROCARDIOGRAPHIC FEATURES: The characteristic sign is incompleteright bundle branch block with rSr pattern in V1 lead. Signs of right ventricularhypertrophy also appear when pulmonary hypertension develops. Atrial fibrillationoccurs in late cases.ECHOCARDIOGRAPHY WITH DOPPLER: Must be done for every patient withsuspected congenital heart disease. In A.S.D. it shows the septal defect and dilatedright ventricle and abnormal movement of the interventricular septum characteristic ofvolume overload on the right ventricle. Cardiac catheterization may be done in somecases.COMPLICATIONS:1- Pulmonary hypertension and reversal of shunt.2- Right ventricular failure. 3- A trial fibrillation.TREATMENT: Small defects can be left alone. Large defects should be closedsurgically or by percutaneous insertion of occluder (device that occludes the ASD) . 26
27. 27. VENTRICULAR SEPTAL DEFECT1- In the presence of a defect in the septum, the right ventricle receives both thenormal venous and the shunted blood. If the defect is big right ventricular hypertrophyoccurs.2- This excessive blood flows in the pulmonary artery and the pulmonary circulationand then returns to the left atrium and the left ventricle. This causes: Dilatation of thepulmonary artery, pulmonary plethora, dilatation of the left atrium, dilatation andhypertrophy of the left ventricle.3- If the shunt is very big excessive flow may cause heart failure in infancy.4- If the shunt is large the pulmonary vessels react by vasoconstriction causingpulmonary hypertension and reversal of shunt (Eisenmenger syndrome).5- Small V.S.D. does not cause pulmonary hypertension and may closespontaneously. Clinically, the murmur is very loud (Roger’s disease).CLINICAL PICTURE: The specific signs of V.S.D. are: 1- A characteristicpansystolic murmur best heart in the third and fourth left intercostal spaces just lateralto the sternum, usually accompanied by a thrill. 2- With large shunts the increasedflow across the mitral valve may cause a third sound and a mid-diastolic flow murmurat the apex.The clinical course depends upon the size of the defect:1- Small ventricular septal defect: many defects close spontaneously.2- Moderately large defect:1st- Progressive pulmonary hypertension and low cardiac output e.g. fatigue,syncope on exercise, pulsations and palpable loud second heart sound in thepulmonary area, right ventricular hypertrophy, etc.2nd- When the pressure in the right ventricle equals that in the left ventricle noblood will flow across the defect and the murmur diminishes disappears. The patientbecomes cyanosed on crying.3rd- When the shunt is reversed the patient becomes cyanosed.X-RAY PICTURE: Is normal in cases with small defects. Large defects result in:pulmonary plethora (overfilled large and tortuous pulmonary arteries), large mainpulmonary artery, left and right ventricular enlargement, left atrial enlargement. 27
28. 28. ECHOCARDIOGRAPHY WITH DOPPLER: Can show the size of cardiac chambers.The defect can sometimes be shown by two-dimensional echo. Color Doppler is veryhelpful in showing the blood flow through the defect. Detection of the site of thedefect, the magnitude of the shunt and the degree of pulmonary hypertension can beassessed by this non-invasive method.CARDIAC CATHETERISATION AND ANGIOGRAPHY: Is done in some cases.COMPLICATIONS: Infective endocarditis, pulmonary hypertension, and heartfailure.DIFFERENTIAL DIAGNOSIS: A pansystolic murmur at the sternal border can becaused by tricuspid or mitral incompetence in addition to the ventricular septal defect.Sometimes the murmur of pulmonary stenosis is heard at the third intercostal spacebut it is usually ejection in type and its maximal intensity is in the second space. Othercauses of systolic murmur at left sternal border are hypertrophic obstructivecardiomyopathy, subaortic membrane and aortic stenosis.TREATMENT:1- To prevent infective endocarditis all patients must receive an antibiotic prophylaxisbefore performing minor procedures that may causes bacteremia, e.g. dentalextraction, delivery, etc.2- Small ventricular septal defects should be left alone. Many of them closespontaneously.3- Surgical closure is indicated if the defect is moderate or large in size, provided thatthe pulmonary pressure is normal or moderately elevated. Surgical closure iscontraindicated if pulmonary pressure is severe (Eisenmenger’s syndrome). PATENT DUCTUS ARTERIOSUSThe ductus arteriosus is normally present in the fetus. It connects the aorta (at thejunction of the arch with the descending aorta) with the pulmonary artery (at thejunction of the main pulmonary artery with its left branch). It normally closes. Duringthe first month after birth:Effects:1- The blood flows through the duct from the aorta to the pulmonary artery, i.e. left toright shunt. 28
29. 29. 2- As the pulmonary artery receives blood both from the shunt and the right ventricle,pulmonary artery dilatation and pulmonary plethora occur.3- If the shunt is big pulmonary vasoconstriction and hypertension occurs. When thepressure in the pulmonary artery equals that of the aorta the shunt will first becomeconfined to the systole only and then ceases altogether. The murmur, accordingly, willfirst become only systolic and finally will be completely inaudible.5- When the pressure in the pulmonary artery exceeds that of the aorta, the shunt willbe reversed and cyanosis occurs (Eisenmenger’s syndrome).CLINICAL FEATURES: Patent ductus arteriosus is commoner in females. Itscharacteristic signs are:1- A continuous (machinery) murmur that occupies both systole and diastolebecause the pressure in the aorta exceeds that of the pulmonary artery all through thecardiac cycle. It is best heard in the first and second left intercostal spaces. There maybe continuous thrill in the same area.2- With large ductus, the increased flow across the mitral may cause a mid-diastolicmurmur.When the pressure in the pulmonary artery exceeds that of the aorta, right to left shuntoccurs and cyanosis appears (Eisenmenger’s syndrome). The deoxygenated blood willflow from the pulmonary artery across the ductus down the descending aorta. Thelower limbs will be cyanosed while the upper limbs remain pink (differentialcyanosis).X-RAY PICTURE: X-ray is normal in cases with small ductus. In moderate to largeductus the following signs appear: Pulmonary plethora, enlargement of the left atrium,left ventricle and the aorta. Hilar dance seen in the hilum by screening.Differential diagnosis: Other causes of continuous murmur as aorto-pulmonarywindow, in coarctation of the aorta, mammary softle, rupture sinus of Valsalva,venous hum...TREATMENT: Prophylaxis against endocarditis. Closure either surgical or with adevice introduced with percutaneous, transvenous catheter. 29
30. 30. CYANOTIC HEART DISEASE- Tetralogy of Fallot.- Ebstein anomaly.- Transposition of the great arteries.- Total anomalous pulmonary venous drainage.- Truncus arteriosus.- Pulmonary arterio-venous malformation. Acquired cyanotic disease: Eisenmenger Syndrome. FALLOT’S TETRALOGYPATHOLOGY AND EFFECTS: Fallot’s tetralogy consists of:1- Severe pulmonary stenosis which causes right ventricular hypertrophy. Thepulmonary stenosis is usually infundibular but sometimes it is both valvular andinfundibular.2- Large ventricular septal defect which makes the pressure equal in both ventricles.3- The origin of the aorta is abnormally deviated to the right (dextroposed, dextro =right) so that it lies partly over the right ventricle (the aorta overrides both ventricles). 30
31. 31. 4- Due to the severe pulmonary stenosis and the large ventricular septal defect, thepressure in both ventricles is equal. There is rush of blood across the defect and theventricular septal defect produces no murmur.5- Part of the blood pumped by the right ventricle passes in the aorta (right to leftshunt) causing central cyanosis. In summary Fallot’s tetralogy consists of four components (tetra =4).1- Pulmonary stenosis.2- Ventricular septal defect.3- Dextroposed and overriding aorta.4- Right ventricular hypertrophy.CLINICAL FEATURES:1- The patient is cyanosed since birth, (usually after birth by few weeks); the degreeof cyanosis depends on the severity of the pulmonary stenosis.2- When the patient exercises, cyanosis is increased. In order to increase the bloodflow to the head and brain, the child usually squats to compress the lower limbsagainst the abdomen and to deviate the blood from the lower to the upper half of thebody. It also increases the systemic arterial resistance. As the pressure in the aortarises, more blood will be deviated across the pulmonary stenosis to the lungs. Thusmore oxygenated blood returns to the heart.3- Chronic cyanosis and tissue anoxia results in: Dyspnea, fatigue, angina, retardedgrowth, polycythemia, clubbing of fingers.4- Sometimes the muscle surrounding the outflow tract of the right ventricle goes intospasm, especially after excitement and exercise. The blood flow to the lungs decreasesmarkedly and the oxygenation decreases resulting in attacks of severe cyanosis:cyanotic spells. If prolonged they may lead to death.5- The characteristic cardiac signs are:A- Murmur of pulmonary stenosis (ejection systolic murmur in second left space, usually accompanied by a thrill.B- The second heart sound is single and consists only of the aortic component. C- Right ventricular hypertrophy.X-RAY PICTURE: 31
32. 32. 4. Right ventricular hypertrophy causes the apex to be displaced outwards andbecomes separated from the diaphragm.5. Right-sided aortic arch in some cases.6. Pulmonary oligemia (the pulmonary artery and its branches are diminished in sizedue to the pulmonary stenosis. All the above factors result in a characteristic cardiacshadow: Coeur en sabot (sabot = wooden shoe).ELECTROACARDIOGRAPHIC FEATURES: Show moderate right ventricularhypertrophy.ECHOCARDIOGRAPHY WITH DOPPLER: Delineates the abnormal anatomy.Cardiac catheterization and angiography is needed for differential diagnosis.COMPLICATIONS:1- Polycythemia causes increased viscosity of blood resulting in a tendencytowards thrombosis, e.g. cerebral thrombosis.2- Infective endocarditis3- Brain abscess results when bacterial emboli are shunted from the venous to thearterial side and lodge in the brain (paradoxical embolism).TREATMENT:1- Surgical correction is indicated in all cases by: Resection of the excessive stenoticinfundibular muscle splitting of the fused pulmonary valve leaflets, and closure of theventricular septal defect.2- If he patient is too young, or the condition is too severe, an anastomosis isperformed to allow blood to reach the lungs by: implanting the subclavian artery inthe corresponding pulmonary artery (Blalock-Taussig operation).3- Cyanotic attacks result from infundibular spasm and constitute an emergency. Theare treated by: Put the patient in the squatting position or compress the flexed lowerlimbs against the abdomen, sedation, propranolol (inderal) intravenously. Propranololis a beta-adrenergic blocker. It depresses the contractility of the infundibular muscle. LEFT VENTRICULAR OUTFLOW TRACT OBSTRUCTION- Valvular aortic stenosis: 70% of patients with valvular AS a malformation of thevalve (usually a bicuspid valve).- Discrete subvalvular aortic membrane:Represents 8-10% of congenital AS. The magnitude of obstruction is variable. Mostmembranes are eventually associated with progressive aortic regurgitation and their 32
33. 33. presence may be an absolute indication for excision. There is a high recurrence rateafter excision (approximately 30% and septal myotomy is often performed). COARCTATION OF THE AORTANarrowing of the aorta usually just distal to the left subclavian artery. Coarctationmay affect other parts of the aorta or the renal arteries.EFFECTS:1- Because of the narrowing, pressure rises in the ascending aorta and the aortic archand its branches. This results in hypertension in the upper limbs.2- Pressure and flow decreases in the descending aorta and its branches producingischemia in the abdominal organs and the limbs.3- Ischemia of the kidneys results in release of renin which raises the blood pressure.4- Hypertension results in left ventricular hypertrophy and it severe results in leftventricular failure.5- Anastomosis form between the branches of the aorta proximal and distal to theobstruction. The most important of these connect the subclavian artery through itsinternal mammary branch to the intercostal arteries which arise from descendingaorta. The intercostal arteries become enlarged and tortuous and erode the lowerborder of the ribs causing rib notching. Appreciable anastomosis develops graduallyby time. That is why rib notching is not detectable except after the age of 10. Otheranastomosis develops around the scapula and another connects the superior andinferior epigastric arteries.CLINICAL FEATURES:1- In the majority of cases there are no symptoms and the essential diagnostic featureof coarctation is that the blood pressure in the upper limbs exceeds that in the lowerlimbs.2- The pulse in the upper limbs, neck and suprasternal notch is strong. Pulse in thelower limbs is weak and delayed or absent.3- Hypertension in the upper half of the body may produce headache, epistaxis whileischemia of the lower half may produce thin, underdeveloped lower limbs andclaudication in the calf. 33
34. 34. 4- Visible and palpable pulsations of dilated collateral may be felt in the intercostalareas.5- A late systolic murmur may be heard on the back due to blood flow in thecollaterals. The murmur is sometimes continuous.6- The cardiac signs are nonspecific and include: left ventricular hypertrophy, anejection systolic murmur heard at the aortic area.X-RAY PICTURE:1- Signs of left ventricular hypertrophy.2- Rib notching is the most specific sign.ELECTROCARDIOGRAPHIC SIGNS: Left ventricular hypertrophy and strain.COMPLICATIONS:1- Hypertension in the upper half of the body may result in: cerebral or subarachnoidhemorrhage, left ventricular failure, dissection of the aorta.2- Infective endocarditis.TREATMENT: surgical resection of the narrowed segment is indicated in moderateand severe cases preferably during childhood. Balloon dilation with expandable stentis a feasible method of treatment. All patients must have prophylaxis againstendocarditis. PULMONARY STENOSISPulmonary stenosis may be caused by: Congenital fusion of pulmonary valve cusps(congenital valvular pulmonary stenosis).EFFECTS:1- In both valvular and infundibular stenosis the pressure in the right ventricle rises,this causes hypertrophy of the right ventricle (pressure over-load). Consequently theright atrium hypertrophies. When the stenosis is severe the output of the rightventricle and the cardiac output are reduced. The pulmonary blood flow is reduced,i.e. pulmonary oligemia.CLINICAL FEATURES:1. Mild cases are as asymptomatic, in severe cases low cardiac output occurs andresults in fatigability, syncope on effort, small volume pulse, cold extremities, etc. 34
35. 35. 2. An ejection systolic murmur is caused by passage of blood through the stenosedvalve. It is best heard over the pulmonary area. It may be preceded by an ejectionclick.3. The pulmonary component of the second heart sound is faint and delayed due toprolonged contraction of the right ventricle.4. There is usually a systolic thrill over the pulmonary area.5. Right ventricular hypertrophy produces a sustained impulse in the third andfourth intercostal spaces just to the left of the sternum and pulsation in theepigastrium. Forceful right atrial contraction causes a large wave in the neck veins(the a wave).X-RAY PICTURE: 1. Pulmonary oligemia occurs in moderate to severe cases andresults in reduced pulmonary vascular markings). 2- Right ventricular enlargement isproportional to the severity of the stenosis. Right atrial enlargement may also occur.3. Post-stenosis dilatation of the pulmonary artery is seen.ECG FEATURES: Right ventricular hypertrophy.ECHO FEATURES: Right ventricular hypertrophy, the stenosed pulmonary valve.TREATMENT: Either percutaneous transvenous balloon dilatation (the standardtreatment, first option) or surgical removal of the valve by open-heart surgery.Interventions In Congenital Heart Diseases (therapeutic procedures that are used intreatment without surgery but through catheterization):- Pulmonary stenosis balloon dilatation.- Aortic stenosis balloon dilatation.- Coarctation of the aorta balloon dilatation and stent insertion.- Atrial septal defect insertion of Amplatzer occluder through catheter.- Patent ductus arteriosus occlusion by insertion of coil.- Other procedures. 35
36. 36. DIAGNOSIS AND MANAGEMENT OF SYNCOPE AND HYPOTENSIONSyncope is a sudden and transient loss of consciousness with associated loss ofpostural tone. The occurrence of syncope is 3% in men ad 3.5% in women in thegeneral population. As a general role, the incidence of syncope increases with age.Hypotension: When systolic blood pressure (SBP) is less than 90 mmHg or reductionof SBP of 30 mmHg or more from baseline.Patients with transient episode of altered consciousness (presyncope) and those withcomplete loss of consciousness (syncope) are classified into 3 broad categories:cardiac syncope, noncardiac syncope, and syncope of undetermined etiology.Among all patients with syncope associated with cardiac disease, sudden cardiacdeath is extremely high. Table: Causes of SyncopeCirculatory (reduced cerebral blood flow)A. Inadequate vasoconstrictor mechanisms1. Vasovagal (vasodepressor)2. Postural hypotension3. Primary autonomic insufficiency4. Sympathectomy (pharmacologic, due to antihypertensive medications such asmethyldopa and hydralazine, or surgical )5. Carotid sinus syncope6. Diseases of the central and peripheral nervous system, including autonomicnerves)B. Hypovolemia1. Blood loss – gastrointestinal hemorrhage.2. Addison’s diseaseC. Mechanical reduction of venous return1. Valsalva maneuver. 2. Cough; Micturition.3. Atrial myxoma, ball valve thrombus.D. Reduced cardiac output1. Obstruction to left ventricular outflow: aortic stenosis, hypertrophic subaorticstenosis. 36
37. 37. 2. Obstruction to pulmonary flow: pulmonary stenosis, primary pulmonaryhypertension, pulmonary embolism.3. Myocardial: massive myocardial infarction with pump failure.4. Pericardial: cardiac tamponadeE. Arrhythmias1. Bradyarrhythmiasa. Atrioventricular (AV) block (second and third degree), with Stokes-Adamsattacksb. Ventricular asystolec. Sinus bradycardia, sinoatrial block, sinus arrest, sick sinus syndromed. Carotid sinus syncopea. Tachyarrhythmias: Supraventricular tachycardia. Episodic ventriculartachycardiaOther causes of disturbances of consciousnessA. HypoglycemiaB. HypoxiaC. HypoventilationD. Transient cerebral ischemic attackE. Emotional disturbances, anxiety attack, hysterical seizures. Noncardiac SyncopeNeurocardiogenic syncope:The syndrome of neurocardiogenic syncope, the common faint (also referred to asneurally mediated hypotension, vasovagal syncope, and vasodepressor syncope), isone of the most common causes of syncope.This disorder is due to abnormality in the neuro-cardiovascular interactionsresponsible for maintaining systemic and cerebral perfusion.Diagnostic evaluation:Head-up tilt (HUT) is essential for the diagnosis of neurocardiogenic syncope. Herewe change the position of the patient from the horizontal to the vertical position. HUTat an angle of 60º to 90º for a time period of 20 to 60 min is the usual protocol.Management of syncope:First-line therapy includes counseling the patient to avoid dehydration, prolongedperiod of standing motionless, and situations known to trigger syncope. Volume 37
38. 38. expansion, fludrocortisone may be helpful in augmenting salt retention and volumeexpansion.Alpha-Agonists: Medodrine may prevent neurocardiogenic syncope due tovasoconstrictor effect that may reduce venous pooling.Orthostatic Syncope (orthostatic Hypotension):Orthostatic hypotension is a disorder in which assumption of the upright posture isassociated with a fall in blood pressure. Therapy: is based on treatment of causes.Management of hypotension: 1- Treatment of the etiology. 2- Avoid dehydration.3- Medodrine. 4. Mineralocorticoids as Astonin H.Cardiac SyncopeIt is due to severe diminution of the cardiac output Either due to severe obstructivelesion as tight mitral stenosis, atrial myxoma, aortic stenosis, obstructivecardiomyopathy or due to arrhythmia whether tachy or brady. Obstructive lesions andarrhythmias frequently coexist; indeed, one abnormality may accentuate the other.Common disorders associated with cardiac syncope are listed in table.Diagnostic evaluation of syncope associated with cardiac disease:- History & physical examination- Echocardiography & Doppler- Standard ECG- Holter monitor ( 24 h. ECG continuous recording )- Electrophysiologic study.- Cardiac catheterization.Treatment of cardiac syncope: Obstructive Heart Disease, for patients with syncopecaused by obstructive heart disease, cardiac surgery is often the treatment of choice.Arrhythmic syncope, detailed discussion of therapy for cardiac arrhythmias presentedearlier. Antiarrhythmic drugs, pacemakers and ablation are available tools ofmanagement of arrhythmia.Syncope of undetermined cause: Despite careful diagnostic evaluation, the cause ofsyncope often cannot be defined. 38
39. 39. Sudden Cardiac DeathDefinition: Sudden cardiac death describes the unexpected natural death due tocardiac cause within a short period from the onset of symptoms.More recent definition focused on time interval of one hour from the symptomsleading to collapse and then to death.Incidence: SCD accounts for 300.000 to 400.000 deaths yearly in the United States.SCD is the most common and often the first manifestation of coronary heart disease(CHD) and is responsible for half the deaths from cardiovascular disease.Sudden Cardiac Death in the young: The most common underlying pathologicalconditions in people who die of SCD in the first three decades of life are myocarditis,hypertrophic cardiomyopathy, congenital coronary artery anomalies,atherosclerotic coronary heart disease, conduction system abnormalities (e.g. longQT), congenital arrhythmogenic disorders, arrhythmias associated with mitralvalve prolapse and aortic dissection. About 40% of SCD in the pediatric populationoccur in patients with surgically treated congenital cardiac abnormalities. Risk factors for Sudden Cardiac Death (SCD):1- Left ventricular hypertrophy (by ECG)2- Cholesterol.3- Hypertension.4- Cigarette smoking.5- Diabetes.6- Alcohol.7- Obesity.8- History of coronary heart disease.9- Age.10- Positive family history of SCD.11- Frequent PVCs (Premature ventricular contractions, unsustained ventriculartachycardia). Cardiac Abnormalities Associated with Sudden Cardiac DeathI. Ischemic heart disease 39
40. 40. A) Coronary Atherosclerosis:- Acute myocardial infarction, - Chronic ischemic cardiomyopathyB) Anomalous origin of coronary arteries.II. CardiomyopathiesA. Idiopathic dilated cardiomyopathyB. Hypertrophic cardiomyopathyC. Hypertensive cardiomyopathyD. Arrhythmogenic right ventricular dysplasiaIII. Valvular heart disease: Aortic stenosisIV. Inflammatory and Infiltrative myocardial diseaseV. Congenital heart disease.VI. Primary Electrical Abnormality.A. Long Q-T syndromeB. Wolf Parkinson White syndrome (WPW).C. Idiopathic ventricular tachycardiaD. Idiopathic ventricular fibrillationE. Brugada syndrome (right bundle block with raised ST in V1 to V3)VII. Drug and other toxic agentsA. Proarrhythmia (Drug induced arrhythmia)B. Cocaine and Alcohol. C. Electrolyte abnormalities Treatment Options for Patients at Risk of Sudden Cardiac Death (SCD)I. Pharmacologic therapy1- Beta blockers , Angiotensin-converting enzyme inhibitors2- Class I antiarrhythmic drugs,3- Class III antiarrhythmic drugs: Amiodarone, sotalolII. Device therapy1- Automatic implantable cardioverter Defibrillator (ICD)2- External automatic defibrillatorIII. Role of surgery: RevascularizationIV. Catheter Ablation therapy. 40
41. 41. CARDIAC ARRHYTHMIASAn arrhythmia is any disturbance in the normal sequence of impulse generation andconduction in the heart.Anatomy of the conduction system: The conduction system of the heart consists ofthe sinus node, internodal tracts, atrioventricular node (AVN), bundle of His, bundlebranches (right and left), and Purkinje fibers. Fig: The pathways of Conduction.General considerations: Normal cardiac impulses arise from the automatic(pacemaking) cells of the sinus node and are conducted through the atria to the AVjunction then the His-Purkinje system to the ventricular muscle. Normally the sinusnode discharges at a rate of 60-100/min. Mechanisms of arrhythmiasA- Disturbance of impulse formation: may result from either:1- Disturbed normal automaticity:2- Triggered activity: Hyper-excitable focus which discharges ectopic impulses.B- Disturbance of Impulse conduction: e.g. heart block Classification of arrhythmia:Clinical classification:- Rapid, regular. Sinus tachycardia, supraventricular tachycardia, atrial flutter,ventricular tachycardia. 41
42. 42. - Rapid, irregular. Sinus arrhythmia, multiple ectopic beats whether atrial orventricular, atrial fibrillation.- Slow, regular. Sinus bradycardia, nodal rhythm, complete heart block.- Slow, irregular. Slow atrial fibrillation. Disturbances in Sinus Rhythm Sinus tachycardiaCardiac impulses arise in the sinus node at a rate more than 100/min.Etiology:A- Physiological: Infancy, childhood, exercise and excitement.B- Pharmacological: Sympathomimetic drugs such as epinephrine and isoproterenol.Parasympatholytic drugs such as atropine. Thyroid hormones, nicotine, caffeine,alcohol.C- Pathological: Fever, hypotension, heart failure, pulmonary embolism,hyperkinetic circulatory states as anemia.Treatment: 1- Treatment of the underlying etiology. 2- Propranolol. Sinus BradycardiaCardiac impulses arise in the sinus node at a rate less than 60/min.Etiology:A- Physiologic: Athletes, sleep, and carotid sinus compression.B- Pharmacologic: Digitalis, propranolol, verapamil and diltiazem.C- Pathologic: Convalescence from infections, hypothyroidism, obstructivejaundice, rapid rise of the intracranial tension, hypothermia and myocardial infarction(particularly inferior wall infarction).Treatment:1- Treatment of the underlying etiology is usually all that is needed.2- If the patient is hemodynamically compromised, Atropine 0.6 – 1.0 mg IV maybe given and repeated every 3 hours (maximum 2.5 mg in two hours).SICK SINUS SYNDROME: This term is applied to a syndrome encompassing anumber of sinus nodal abnormalities that include: 1- persistent spontaneous sinusbradycardia not caused by drugs, and inappropriate for the physiologicalcircumstance, 2- apparent sinus arrest or exit block, 3- combinations of SA and AV 42
43. 43. conduction disturbances, or 4- alternation of paroxysms of rapid and slow atrial andventricular rates (bradycardia-tachycardia syndrome). FIG. Normal intracardiac electrograms. PREMATURE BEATS (EXTRASYSTOLES)These are cardiac impulses of ectopic origin occurring earlier than expected in theprevailing rhythm. The ectopic focus may be: 1- Atrial resulting in atrial prematurebeat. 2- AV junctional (arising from bundle of His) resulting in AV junctionalpremature beat. 3- Ventricular resulting in ventricular premature beat.Etiology:A- Physiological: Emotions, exercise and fatigue.B- Pharmacological: Coffee, alcohol, tobacco, catecholamines, digitalis and hypoxia.C- Pathological: Various infections, digestive disturbances, hyperthyroidism and allcardiovascular disorders. 43
44. 44. SUPRAVENTRICULAR TACHYARRHYTHMIASAll tachyarrhythmias that originate above the bifurcation of the bundle of His areclassified as supraventricular arrhythmias (SVT). The atrial rate must be 100 or morebeats per minute for a diagnosis.SVTs may be separated into three groups based on duration: brief paroxysms,persistent, and chronic (permanent).Arrhythmias that are paroxysmal in onset and offset (e.g., paroxysmal SVT due to AVnodal reentry or WPW syndrome, paroxysmal atrial fibrillation, paroxysmal atrialflutter) tend to be recurrent and of short duration; i.e., seconds to hours.Persistent tachycardias (e.g., sinus tachycardia, ectopic atrial tachycardia(nonparoxysmal), multifocal atrial tachycardia, longer episodes of PSVT or atrialflutter or fibrillation) may persist for days or weeks.Longstanding or chronic SVTs (chronic atrial flutter, chronic atrial fibrillation) do notrevert if untreated, often fail to revert even with attempted treatment, and if revertedwill frequently recur despite therapy.Supraventricular tachyarrhythmias include; atrial tachycardia, atrial flutter, atrialfibrillation and AV tachycardias. ATRIAL FLUTTERAtrial flutter is a rapid regular atrial tachyarrhythmia that is less common than thePSVTs or atrial fibrillation. It is observed in the presence of underlying atrialabnormalities such as those secondary to mitral valve disease, congenital heartdisease, cardiomyopathies, and, less frequently, coronary artery disease.Untreated atrial flutter usually has atrial rates between 240 and 340 per minute,commonly very close to 300 per minute. The ventricular rate in atrial flutter is usuallya defined fraction of the atrial rate 2: 1 conduction generating a ventricular rate of 150per minute and 4:1 conduction at 75 per minute.Clinically, atrial flutter may occur in brief, persistent, or chronic forms, andtherapeutic approaches are influenced by the clinical pattern.Electrocardiographic Features 44
45. 45. Atrial flutter generates a defined pattern of atrial activity in the ECG. Classically, asaw-tooth pattern is identifiable in leads II, 111, and aVF. A narrow QRS complextachycardia at a rate of 150 per minute should always lead to the consideration ofatrial flutter. Carotid sinus massage will not interrupt atrial flutter but nonethelessmay be very helpful in distinguishing flutter from other mechanisms, impairment ofAV nodal conduction causes an abrupt change from a rate of 150 per minute to 75 perminute or less.Management of atrial flutter: - If the patient is hemodynamically compromised,D.C. cardioversion using low energies (around 50 joules) should be instituted.- Administering a Class IA antiarrhythmic agent (i.e., quinidine, procainamide, ordisopyramide). IC antiarrhythmic drugs, flecainide and propafenone, are as effective,if not more effective than Class IA drugs. Class III antiarrhythmic agents (i.e.,amiodarone, sotalol) may also be quite effective. In general, atrial flutter is difficult tosuppress completely with drug therapy. - The ventricular rate is slowed by digitalisand/or propranolol or verapamil before antiarrhythmics are instituted to avoid veryrapid rates associated with drug induced 1:1 AV conduction.- At present, catheter ablation provides the best hope of cure.FIG. A 12-lead ECG of a typical case of type 1 atrial flutter. FIG. A 12-lead ECG of a typical case of type 1 atrial flutter. 45
46. 46. FIG: Atrial flutter with AV block varying between 2: 1 and 4: 1. AV Nodal Reentrant TachycardiaElectrocardiographic Features: Paroxysmal SVT due to AV nodal reentry ischaracterized by an abrupt onset and termination and usually has a narrow QRScomplex without clearly discernable P waves. The rate is commonly in the range of150 to 250 per minute (commonly 180 to 200 bpm in adults) and with a regularrhythm.Management of PSVT Due to AV Nodal ReentryThe acute attack: Vagal maneuvers serve as the first line of therapy. Simpleprocedures to terminate paroxysmal SVT- Carotid sinus massage: If effective the rhythm is abruptly stopped; occasionallyonly moderate slowing occurs- Cold water splash on face.- Performance of Valsalvas maneuver (often effective).Intravenous adenosine, Ca channel blockers (verapamil), digoxin or B-blockers arethe choices for managing the acute episodes.Adenosine, 6 mg given intravenously, followed by one or two 6-mg boluses ifnecessary, is effective and safe for acute treatment. 46
47. 47. A 5-mg bolus of verapamil (isoptin) , followed by one or two additional 5-mgboluses 10 min apart if the initial dose does not convert the arrhythmia, has been aneffective regimen in up to 90 percent of patients with PSVT due to AV node reentry.Intravenous digoxin, 0.5 mg infused over 10 min and repeated if necessary mayconvert the arrhythmia.DC cardioversion: Consider DC cardioversion before digitalis or a beta blocker isadministered.Radiofrequency catheter ablation: Should be considered early in the managementof patients with symptomatic recurrent episodes of AV node reentry. AV Reentrant Tachycardia PSVT Due to Accessory Pathways (The Wolff-Parkinson-White Syndrome)ELECTROCARDIOGRAPHIC RECOGNITION: Three basic features in the ECG ofpatients with the usual form of WPW syndrome caused by an AV connection:(1) Short P-R interval less than 120 msec during sinus rhythm; 47
48. 48. (2) QRS complex duration exceeding 120 msec(3) Slowly rising onset of the QRS in some leads (delta wave).The most common tachycardia is characterized by a normal QRS, by ventricular ratesof 150 to 250 beats/min and by sudden onset and termination.Termination of the acute episode should be approached as for AV nodal reentry. Inmany patients, particularly those with a very rapid ventricular response, electricalcardioversion is the initial treatment of choice. The Wolff-Parkinson-White SyndromeELECTRICAL ABLATION: Ablation of the accessory pathway is advisable forpatients with frequent symptomatic arrhythmias that are not fully controlled by drugs. Atrial FibrillationThe arrhythmia is characterized by multiple electric foci in the atrium causingdisorganized atrial depolarizations without effective atrial contraction. Electricalactivity of the atrium can be detected on ECG as small irregular baseline undulations, 48
49. 49. called f waves, at a rate of 350 to 600 beats/min. The ventricular response is grosslyirregular (irregular irregularity) and is usually between 100 and 160 beats/min.It is a common arrhythmia, occurring in 5 – 10 % of individuals over 65 years of age.It also occurs in a paroxysmal form in younger patients.The hemodynamic consequences of atrial fibrillation are due to two factors:(1) The loss of atrial systole may impair ventricular function in the noncompliantventricle [e.g., aortic stenosis, left ventricular hypertrophy (LVH)] or the dilatedventricle with systolic dysfunction, and(2) A rapid ventricular rate will encroach upon the diastolic filling period of the leftventricle and the diastolic flow time of the coronary arteries.(3) The risk of embolism and stroke is a long-term concern of special importance.Atrial fibrillation may occur in paroxysmal, persistent, and chronic patterns.Clinical expression of atrial fibrillation:Definition Duration- Paroxysmal Minutes/hours- Short-lasting Seconds --<1 hour- Long-lasting >1 hour; -- < 48 hours- Persistent Two days -- weeks- Permanent (Chronic) Months / yearsTable: Causes of atrial fibrillationWith structural heart disease- Rheumatic mitral valve disease- Ischemic heart disease- Hypertension- Cardiomyopathy: Dilated, Hypertrophic- Atrial septal defect, - Constrictive pericarditis, MyocarditisWithout structural heart disease- Alcohol. Thyrotoxicosis- Acute pericarditis. Pulmonary embolism- Sick sinus syndrome, Lone atrial fibrillation 49
50. 50. Atrial FibrillationClinical pictureOnset and offset are sudden in paroxysmal cases.Symptoms: Paroxysmal AF produces symptoms similar to those of supraventriculartachycardia. Established AF (persisting for more than two weeks) is better toleratedthan the paroxysmal variety. Congestive heart failure may occur if the attack isprolonged, the ventricular rate is very rapid, or the underlying heart disease is severe.Signs:1- Arterial pulse:a- Rate is usually 100-150/min. Slower rates may be encountered in old age and inpatients receiving digitalis or beta-blockers.b- Rhythm shows marked (irregular) irregularity. c- Force is irregular. d- Pulsusdeficit: The radial pulse rate is less than the cardiac rate counted at the apex beat. Thisis due to inability of the week ventricular contractions following short diastolicperiods to open the aortic valve. 50
51. 51. 2- Neck veins show systolic expansion; no “a” waves are seen.3- Auscultation reveals varying intensity of S1.4- Exercise increases the pulse irregularity and deficit.Electrocardiogram: The P waves are replaced by irregular f waves. The QRScomplexes are normal in shape but irregularly spaced.Complications: 1- Atrial thrombosis due to stagnation of blood in the fibrillatingatria. The formed thrombi may embolize in the systemic and pulmonary circulations.2- Heart failure due to loss of the atrial contribution to contractility and the cardiacoutput. Atrial fibrillation (AF) progressed to ventricular fibrillation (VF) Treatment of Atrial FibrillationPharmacologic Management of Patients with Recurrent Persistent or Permanent AF:- Recurrent Persistent AF:A) Minimal or no symptoms: Anticoagulation and rate control as needed.B) Disabling symptoms in AF:1- Anticoagulation and rate control2- Antiarrhythmic drug therapy3- Electrical cardioversion as needed, continue anticoagulation as needed andtherapy to maintain sinus rhythm- Permanent AF: Anticoagulation and rate control as needed. 51
52. 52. Antiarrhythmic Drug Therapy to Maintain Sinus Rhythm in Patients withRecurrent Paroxysmal or Persistent AF:A) No or minimal heart disease:1- Flecainide, propafenone, sotalol2- Amiodarone, dofetilide, Disopyramide, procainamide, quinidine3- Consider non-pharmacological options.B) Heart disease present:a- Heart failure: Amiodarone, dofetilide1- Coronary artery disease: Sotalol, Amiodarone, dofetilideC) Hypertension: With1- With LVH (septum greater than or equal to 1.4 cm): Amiodarone2- Without this degree of LVH: - Flecainide, propafenone.FIG. General scheme to select antiarrhythmic drug therapy for the prevention ofatrial fibrillation. HPB, hypertension; CHF, congestive heart failure; CAD, coronaryartery disease; CR, controlled release; AF, atrial fibrillation.Drugs for Pharmacologic Cardioversion of AF (Rhythm control): Drug Route of Admin. And Dosage Amiodarone Oral: 1.2 to 1.8 g /day then 200 to 400 mg /d maintenance. Propafenone Oral: 450 to 600 mg Quinidine Oral: 0.75 to 1.5 g in divided doses over 6 to 12 h usually with a rate-slowing drug. 52
53. 53. Oral Pharmacological Agents for Heart Rate Control in Patients with AF: Drug Maintenance dose Digoxin 0.125 to 0.375 mg daily Diltiazem 120 to 360 mg daily in divided doses Metoprolol* 25 to 100 BID Verapamil 120 to 360 mg daily in divided doses* Other beta-blockers could be used in appropriate doses Anticoagulation of Patients with Atrial Fibrillation: IndicationsRheumatic mitral valve disease with recurrent or chronic atrial fibrillation.Dilated cardiomyopathy with recurrent persistent or chronic atrial fibrillation.Prosthetic valves.Prior to (>3 weeks) elective cardioversion of persistent or chronic atrial fibrillation,and also for 3 weeks after cardioversion (because of atrial stunning).Coronary heart disease or hypertensive heart disease with recurrent persistent orchronic atrial fibrillationAtrial fibrillation in thyrotoxicosis (while awaiting long-term control; electivecardioversion)Chronic or persistent lone atrial fibrillation, age >60 yearsControversial; or limited dataCoronary or hypertensive heart disease with normal left atrial size, after first episodeof paroxysmal atrial fibrillationElective cardioversion of atrial fibrillation of short duration (2-3 days) with normalleft atrial sizeChronic or persistent lone atrial fibrillation, age <60 yearsNot indicatedLone atrial fibrillation, short paroxysms (<48 h)Most clinical settings associated with short paroxysms (minutes to hours)Relative contraindicationsDifficulty controlling prothrombin times. DementiaMalignancies, especially associated with bleeding riskPrior major bleeding events. Uncontrolled hypertension 53
54. 54. Treatment of Cardiac Arrhythmias with Catheter Ablative TechniquesRadiofrequency ablation destroys tissue by controlled heat production. Catheterablation is used to treat patients with four major tachyarrhythmias: atrialflutter/fibrillation, AV nodal reentry, accessory pathways and ventricular tachycardia. VENTRICULAR TACHYCARDIASpecific Forms of Ventricular TachycardiaDuration: Salvo (3-5 impulses)Nonsustained VT: (6 impulses, up to 29 seconds)Sustained VT: (>30 seconds)The electrocardiographic diagnosis of ventricular tachycardia is suggested by theoccurrence of a series of three or more bizarrely shaped premature ventricularcomplexes whose duration exceeds 120 msec, with the ST-T pointing opposite to themajor QRS deflection.The rates range from 70 to 250 beats/min. Ventricular tachycardia can be sustained,defined arbitrarily as lasting longer than 30 sec or requiring termination because ofhemodynamic collapse, or nonsustained (Unsustained), when it stops spontaneouslyin less than 30 sec. Ventricular tachycardia (Wide QRS tachycardia)Management: Intravenous lidocaine or amiodarone, followed by an infusion of thesuccessful drug. If the arrhythmia does not respond to medical therapy, electrical DCcardioversion can be employed. 54
55. 55. Ventricular tachycardia in a patient with right ventricular dysplasia. CONGENITAL LONG QT INTERVAL SYNDROMEThe normal QT interval is .43 sec. The congenital long QT interval syndrome, whichis present persistently from childhood, is characterized by the presence of long QTintervals on the standard 12-lead ECG. The affected patients are prone to episodes oftorsade de pointes (ventricular tachycardia with special polymorphicconfiguration), which may cause transient light-headedness or syncope or suddencardiac death. Arrhythmias may occur at rest, under emotional stress, or with exercise. ACQUIRED LONG QT INTERVAL SYNDROMECauses: Antiarrhythmic drugs as quinidine. There is a growing list of other drugs thatmay prolong the QT interval, and establish susceptibility to torsade de pointes. Theseinclude the phenothiazines, certain antibiotics, pentamidine, cocaine, and terfenadine,among others.Management of Congenital Long QT Interval Syndrome: Long-term therapy includesB-adrenergic blockade. Placement of an ICD should be considered for patients withresistant arrhythmias. 55
56. 56. CARDIOVERSION AND DEFIBRILLATION Differences between cardioversion and defibrillation: Cardioversion Defibrillation Elective Emergency Synchronized Non-synchronized For AF, A. flutter, SVT, VT For V. fibrillation 50, 100, 150, 200 Joules Start by 200 Joules Need sedative first Patient is unconscious VENTRICULAR FLUTTER AND FIBRILLATIONMANAGEMENT: Immediate nonsynchronized DC electrical shock using 200 to 360joules is mandatory treatment for ventricular fibrillation. Cardiopulmonaryresuscitation is employed only until defibrillation equipment is ready. Time shouldnot be wasted with cardiopulmonary resuscitation maneuvers if electricaldefibrillation can be done promptly. The Implantable Cardioverter Defibrillator (ICD)Apparatus (pacemaker) that gives electric shock if the patient develops ventricularfibrillation. The pacemaker is inserted in the sub-pectoral area.ICD indicationsA. Cardiac arrest not due to acute ischemia or infarction or reversible causes.B. Documented sustained VT with hemodynamic compromise.C. Syncope of unknown origin in structural heart disease patients with induciblesustained VT.D. Cardiomyopathy ischemic or non-ischemic with ejection fraction 30% or lower(MADIT II results). AV HEART BLOCKHeart block is a disturbance of impulse conduction that can be permanent or transient,owing to anatomical or functional impairment.The conduction disturbance is classified by severity in three categories. 56
57. 57. During first degree heart block, conduction time is prolonged but all impulses areconducted (P-R interval > 0.2 sec.).Second degree heart block occurs in three forms:Mobitz type I (Wenckebach) and type II; and persistent 2:1 block.Mobitz Type I heart block is characterized by a progressive lengthening of theconduction time until an impulse is not conducted (Fig).Mobitz Type II heart block denotes occasional (Mobitz II) or repetitive sudden blockof conduction of an impulse without prior measurable lengthening of conduction time.When no impulses are conducted, complete or third degree block is present. Mobitz type I (Wenckebach) block Mobitz Type II second degree heart block COMPLETE AV BLOCKELECTROCARDIOGRAPHIC RECOGNITION: Complete AV block occurs whenno atrial activity conducts to the ventricles and therefore the atria and ventricles arecontrolled by independent pacemakers. Thus, complete AV block is one type ofcomplete AV dissociation.The ventricular focus is usually located just below the region of block, which can beabove or below the His bundle bifurcation. The ventricular rate of acquired completeheart block is less than 40 beats/min but may be faster in congenital complete AVblock.CLINICAL FEATURES. Block proximal to the His bundle generally exhibits normalQRS complexes and rates of 40-60 beats/min because the escape focus that controlsthe ventricle arises in or near the His bundle. 57