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Inferior wall infarcts represent nearly half of all ST-segment elevation MI 9 Data from the prethrombolytic era suggests that heart block occurs in approximately 20% of patients with acute inferior myocardial infarction and is associated with a marked increase in mortality2 Although the reported incidence of CAVB with AMI is lower in the thrombolyticÂ era than in the pre thrombolytic era . Mortality associated with CAVB is still high and has not decreased over the lastÂ decade. The AMI patients who develop CAVB have significantly worse prognosis than those patients without CAVB 12 According to TIMI II trial Heart block developed in 12%; 6.3% had heart block on presentation and 5.7% developed heart block within 24 h after treatment with rt-PA. Patients with heart block at entry were slightly older and a greater proportion had cardiogenic shock. The 21-day mortality rate among patients with heart block at entry was 7.1%, compared with 2.7% among patients without heart block (relative risk 2.6, p = 0.007. Among patients without heart block, coronary angiography among patients randomly assigned to coronary catheterization 18 to 48 h after admission revealed that the infarct-related artery was occluded in 28..2% of patients who developed heart block versus 15.5% of patients without heart block (p = 0.04). The 21-day mortality rate was increased among patients in whom heart block developed after thrombolytic therapy (9.9% versus 2.2% of patients without heart block, relative risk 4.5, p less than 0.001).2
DEFINITION OF MI
Criteria for acute myocardial infarction according to American heart association is 13
"The term myocardial infarction should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia. Under these conditions any one of the following criteria meets the diagnosis for myocardial infarction:
Detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value above the 99th percentile of the upper reference limit (URL) together with evidence of myocardial ischemia with at least one of the following:
Symptoms of ischemia
ECG changes indicative of new ischemia (new ST-T changes or new left bundle branch block [LBBB])
Development of pathological Q waves in the ECG
Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
Sudden, unexpected cardiac death, involving cardiac arrest, often with symptoms suggestive of myocardial ischemia, and accompanied by
presumably new ST elevation, or new LBBB, and/or evidence of fresh thrombus by coronary angiography and/or at autopsy, but death occurring
before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood.
For percutaneous coronary interventions (PCI) in patients with normal baseline troponin values, elevations of cardiac biomarkers above the 99th percentile URL are indicative of peri-procedural myocardial necrosis. By convention, increases of biomarkers greater than 3 x 99th percentile URL have been designated as defining PCI-related myocardial infarction. A subtype related to a documented stent thrombosis is recognized.
For coronary artery bypass grafting (CABG) in patients with normal baseline troponin values, elevations of cardiac biomarkers above the 99th percentile URL are indicative of peri-procedural myocardial necrosis. By convention, increases of biomarkers greater than 5 x 99th percentile URL plus either new pathological Q waves or new LBBB, or angiographic ally documented new graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium have been designated as defining CABG-related myocardial infarction.
Pathological findings of an acute myocardial infarction.
Criteria for prior myocardial infarction:
Any one of the following criteria meets the diagnosis for prior myocardial infarction:
Development of new pathological Q waves with or without symptoms.
Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract, in the absence of a non-ischaemic cause.
Pathological findings of a healed or healing myocardial infarction." 13
The pathophysiology of acute MI involves narrowing of epicardial blood vessels as a result of atheromatous plaques. Exposure of the basement membrane due to plaque rupture results in aggregation of platelets, thrombus formation along with accumulation of fibrin and haemorrhage into the plaque, with varying degree of vasospasm. This leads to partial or complete blood vessel occlusion and myocardial ischemia. Total occlusion of the vessel for more than 4-6 hours would cause irreversible necrosis of myocardium, however early reperfusion can salvage the myocardium and decrease morbidity and mortality.
Stimulation of nerve fibres in an ischemic zone of myocardium surrounding the necrotic central area of infarction is thought to gives rise to the pain.
Almost all myocardial infarctions result from coronary atherosclerosis, with superimposed coronary thrombosis. Non atherogenic forms of coronary artery disease include:
Arteritis which may due to
Granulomatous such as Takayasu disease,
Systemic lupus erythematosis, Kawasaki syndrome, Polyarteritis nodosa
Rheumatoid spondylitis, disseminated lupus and, Ankylosing spondylitis
Trauma to coronary arteries
Thrombosis, laceration, or Radiation therapy for neoplasia.
Coronary wall thickening due to metabolic disease or due to intimal proliferative disease
Amyloidosis, Homocystinuria and, Mucopolysaccharidoses,
Hyperplasia of intimal as a result of contraceptive steroids use or during the postpartum period
Other mechanisms causing Luminal narrowing
Prinzmetal angina along with normal coronary vessels.
Aortic dissection or dissection of coronary artery.
Coronary artery emboli.
Nonbacterial thrombotic endocarditis, infective endocarditis.
Mural thrombus arising from left atrium, pulmonary veins or left ventricle.
Prosthetic heart valve emboli. Atrial myxoma
Precipitated by cardiopulmonary bypass as well as coronary arteriography
Thrombi from intracardiac catheters or Paradoxical emboli
Congenital Anomalies of Coronary Artery
Anomalous left coronary artery origin from pulmonary artery
Aneurysm of Coronary artery
Disproportion between Myocardial Oxygen Supply and demand
Aortic stenosis, Takotsubo cardiomyopathy, Aortic insufficiency
Thyrotoxicosis, Hypotension for a prolonged period
In situ Thrombosis,
Disseminated intravascular coagulation,
Polycythemia Vera, TTP (Thrombocytopenic purpura), Hypercoagulable state
Include Cocaine abuse
The patient's history is of utmost importance in making a diagnosis of MI.
PRODROMAL SYMPTOMS. Include:
Which occurs either with mild exertion or at rest (unstable angina)? Often patients will fail to seek medical attention as the chest discomfort is not severe enough and patients tend to ignore its significance.
Generalized fatigue and lethargy often accompanies other symptoms preceding STEMI.
Symptoms may present differently in women than in men and may also have different presentation in elderly than younger population.
In majority of cases, pain is extremely severe in intensity, excruciating and crushing. It can also present as stabbing knifelike discomfort. The patient often experiences a sense of a heavy weight or tightness in the chest.
The pain usually lasts for more than 30 minutes and may be prolonged for couple of hours.
The pain is usually retrosternal initially and spreads to both sides of the anterior chest, more so to the left side. It may also radiate down the left arm on medial aspect with burning, tingling sensation in the left hand, and fingers. The discomfort may radiate to, upper extremities, neck, jaw, between the shoulders, usually towards the left side.
The pain of MI, in some cases is localized in epigastrium especially in cases of inferior MI, mimicking acute abdomen and may also mislead to incorrect diagnosis of dyspepsia.
The pain of myocardial infarction is similar in character and location to that of angina in patients already having angina pectoris, but, it is much more intense, lasts longer, and is not relieved by rest and nitro-glycerine. Opiates, in particular morphine, alleviate the pain.
The pain is often suddenly relieved when blood flow to the infarct territory is restored. In patients in whom reocclusion occurs after fibrinolysis, pain recurs if there is viable myocardium. Thus the "pain of infarction," represents pain caused by ongoing ischemia. This concept envisages the importance of the endeavour to relieve the ischemia, for which the pain is a marker. This finding also suggests that the treating physicians should not take lightly ongoing cardiac pain under any circumstances.
In elderly, diabetic patients, and heart transplantation recipients, STEMI has not the typical course initiating with chest pain and discomfort but rather it may present with symptoms of acute left ventricular failure or by profound weakness or syncope. Diaphoresis, nausea, and vomiting may accompany these symptoms.
Nausea vomiting and sweating usually accompany other symptoms, probably because of stimulation of left ventricular receptors as part of the Bezold-Jarisch reflex or activation of the vagal reflex. Moreover, nausea and vomiting are common side effects of opiates. These symptoms are more frequent in inferior STEMI than anterior STEMI.
Other symptoms include feelings of profound weakness, dizziness, palpitations, cold perspiration, and a sense of impending doom.
On occasion, symptoms arising from an episode of cerebral embolism or other systemic arterial embolism herald a STEMI.
Chest discomfort may not accompany these symptoms.
No physical findings are diagnostic of acute MI. The physical examination can be entirely normal or may reveal only nonspecific abnormalities.
An S4 gallop may be found occasionally. Blood pressure is initially often elevated, but it may be normal or low.
Tachycardia and hypertension (signs of sympathetic hyperactivity) often accompany anterior wall MI, whereas bradycardia and hypotension (signs of parasympathetic hyperactivity) are more common with inferior wall MI.
Vital signs and status of peripheral perfusion should be sought. Signs of both left and right sided cardiac failure, including S3 gallop, pulmonary congestion, and elevated neck veins) should be looked for.
Careful assessment for presence or absence of arrhythmias and mechanical complications (e.g., new murmurs) is also necessary.
In case if evidence of hypoperfusion is present its underlying aetiology whether volume depletion, right heart failure, left heart failure should be determined as it is significantly affects management.
Obtaining ECG is one of the fore most steps in evaluating a patient with chest pain. ECG is also useful in identifying those patients at highest risk of complications following MI14 Serial ECG tracings improve both the sensitivity and specificity of the ECG in making the diagnosis of acute MI and also assist in assessing the outcomes of therapy. The diagnosis of acute MI can be made with certainty when typical ST segment elevation is present and persists for hours, followed within hours to days by T wave inversions and Q waves.
The ECG changes in ST segment elevation acute MI have three overlapping phases in evolution:
(1) Hyper acute or early acute, (2) evolved acute and (3) Chronic (stabilized).
Early Acute Phase
This earliest phase begins within minutes, persists, and evolves over hours. T waves increase in amplitude and widen over the area of injury (hyper acute pattern). ST segments evolve from concave to a straightened to a convex upward pattern (acute pattern). When prominent, the acute injury pattern of blended ST-T waves can take on a "tombstone" appearance. ST segment depressions that occur in leads opposite those with ST segment elevation are known as "Reciprocal changes" and are associated with larger areas of injury and a worse prognosis but also with greater benefits from recanalization therapy.
Evolved Acute Phase
During the second phase, ST segment elevation begins to regress, T waves in leads with ST segment elevation become inverted, and pathologic Q or QS waves become fully developed (>0.03-second duration and/or depth >30% of R wave amplitude)
Resolution of ST segment elevation is quite variable. It is usually complete within 2 weeks of inferior MI, but it can be delayed further after anterior MI. Persistent ST segment elevation, often seen with a large anterior MI, is indicative of a large area of akinesis, dyskinesis, or ventricular aneurysm. Symmetrical T wave inversions can persist for an indefinite period, but usually resolves over weeks to months. Age of an MI in the presence of T wave inversions is often indeterminate. Q waves usually disappear after inferior wall MI but commonly do not resolve after anterior MI.
Early thrombolysis and reperfusion accelerates the resolution of ECG changes so that, on recanalization, the pattern of ECG changes can evolve from one phase to other over minutes to hours instead of days to weeks. ST segments recede rapidly, T wave inversions and losses of R wave occur earlier, and Q waves may not develop or progress and occasionally may regress. Indeed, failure of ST segment elevation to resolve by more than 50 to 70% within 1 to 2 hours suggests failure of fibrinolysis and should be followed by urgent angiography for "rescue angioplasty."
Extent of the infarctÂ -Â
The pattern of ECG abnormalities gives useful information regarding the extent of infarct. For instance, ST segment elevation in leads V5 to V6 >2mm in accompany with an inferior wall MI is 94% sensitive and 98% specific sign of an extensive area of involved inferior and lateral wall myocardium as well as large infarct-related artery. 16
The extent of the infarct may have impact on T wave evolution. T waves that are persistently negative with Q waves for more than one year are usually associated with a transmural MI with entire wall fibrosed; in contrary , T waves that are positive in leads with Q waves are usually indicative of a non transmural MI having viable myocardium in its wall 17. Negative T wave that resolve is also predictive of recovery of regional left ventricular dysfunction. It is uncommon for ECG to completely normalize following Q wave MI but can occur, particularly in case of smaller infarcts especially when regional wall motion and left ventricular ejection fraction improves. The latter changes are mostly associated with good collateral circulation or spontaneous recanalization 18 On the other hand, presence of persistent Q waves as well as ST elevations few weeks after an myocardial infarction have strong correlation with a extensive wall motion disorder either (dyskinetic or akinetic region), although it may not necessarily implement a frank aneurysm of ventricular wall.
ECG IN DIAGNOSIS OF INFERIOR MI
Â ST segment changes or Q waves in leads II, III, and aVF suggest inferior wall ischemia or infarction.
Proximal occlusion of the right coronary artery before the acute marginal branch can cause RV as well as inferior acute MI in about 30% of cases.
Right-sided leads, especially V3R and V4R must also be obtained to assess for possibility of right ventricular ischemia/infarction in case of inferior wall MI.
Because the presence of RV infarction has great impact on the prognosis and treatment of inferior MI, it is important to make this diagnosis. Acute ST segment elevation of at least 1 mm (0.1 mV) in one or more of leads V4R to V6R is both sensitive and specific (>90%) for diagnosing acute RV injury, and Q or QS waves effectively identify RV infarction.
Posterior wall MIÂ -
True posterior wall MI represents a mirror-image ECG pattern of injury in leads V1 to V4. The acute phase is significant for ST segment depression, instead of ST segment elevation.
Acute posterior wall MI is also characterized by elevations of ST segment in leads that are placed over back of the heart, i.e. leads V7 to V9 (oesophageal leads.)14-15. Concomitant ST elevation may also be present in the inferior leads (II, III, aVF), depicting inferior wall MI. Reciprocal depression of ST segment may be present in the anterior leads (e.g., V1-V3). Similar ST changes are also characteristic of ischemia of anterior sub-endocardial wall that may occur in combination with inferior infarction. Postero-inferior wall MI can be differentiated from anterior wall ischemia by the presence of ST segment elevations in the inferior (II, III, aVF) and posterior leads V7 to V9. 9,12,14. Relatively tall R waves may also appear in leads V1-V3), corresponding to the appearance of pathologic Q waves (loss of depolarization forces) in the posterior leads.
IDENTIFICATION OF THE INFARCT-RELATED ARTERYÂ -
Â The ECG may also attribute useful information pertaining to the identification of infarct related artery in patients with an ST elevation MI 21
Inferior MIÂ -
Â Patients having an inferior wall MI have involvement of either the right coronary artery or the left circumflex coronary artery:
ST segment elevation exceeding in lead III than that of lead II, especially when associated with ST depression in leads I and aVL, is reported to be a very useful predictor of an occlusion of either proximal or the mid portion of the right coronary artery. 19-21
However, recent literature suggests that the sensitivity of this sign may only be 70 percent, with specificity of about 72 %21 ST segment elevation in lead II, equal to that of lead III, when accompanied with ST depression in leads V1 to V3 or ST elevation in leads I and aVL, is a useful but not absolute predictor of a left circumflex coronary artery occlusion; as these findings may also be seen in distal occlusion of a dominant right coronary artery 19-21
In a study of 109 patients having an inferior wall MI undergoing angiography, the evidence of concomitant precordial ST segment depression was found to be a sensitive, indicator of left circumflex occlusion; but not specific. It was also observed that, absence of ST segment depression in precordial leads
had a significantly high negative predictive value for excluding the left circumflex artery as the culprit vessel 12
Patients with inferior MI may have right-sided ST elevation in leads V1 and V4R; predictive of acute right ventricular injury 19, 23Â and closely correlates with proximal right coronary artery occlusion. In one study, ST elevation in V4R was 88 percent sensitive and 78 percent specific for coexisting right ventricular infarction.
Right Ventricular Infarction
About 50 percent of patients with inferior infarction have some right ventricle involvement.17,18,22-25 among these patients, right ventricular infarction occurs mainly in patients with transmural infarction of the infero posterior wall and the posterior portion of the septum. Right ventricular infarction invariably occurs in accompany with infarction of inferior left ventricular walls and the adjacent septum, however isolated infarction of the right ventricle is also seen in 3 to 5 percent cases of MI on autopsy.
Right ventricular infarction is less common than would be anticipated from the frequency of atherosclerotic lesions involving the right coronary artery. This discrepancy is due to lower oxygen demands of the right ventricle as right ventricular infarcts occur more frequently in conditions requiring increased right ventricular oxygen needs as for example pulmonary hypertension and right ventricular hypertrophy. Also, the right ventricle has richer inter coronary
collateral system than that of the left, and the presence of thin right ventricular walls allows the chamber to get some nutrition from the blood flowing within its cavity. Therefore the right ventricle can sustain long periods of ischemia but still demonstrate excellent recovery of contractile function after reperfusion.26
Statistics show that Eighty eight percent of the patients having RVMI and 75% with inferior MI without RV involvement have some type of arrhythmia. AV block occurred in 42% of the infarctions with RV involvement and only in 29% of the inferior MI without RV involvement. In 27% of patients with RVMI it was necessary to implant a pacemaker as compared to 10% in inferior MI without RV involvement. Mortality was observed to be higher in the patients with inferior infarction extending to the RV (15.3% vs 3.5%., P= 0.0001). Thus patients having inferior MI with concomitant RV myocardial involvement are at increased risk of death and arrhythmias 07
In a study carried out at PUNJAB (Lahore), the mortality was 33.3% with right ventricle involvement as compared with 2.6% without right ventricle involvement. (p=0.003) in patients with inferior MI. The conclusion being that right ventricle involvement is an independent predictor of prognosis acute inferior myocardial infarction.
Right ventricular infarction can present with a range of clinical features i.e. from mild right ventricular dysfunction through cardiogenic shock.27 Patients with clinically significant right ventricular infarction show a characteristic
hemodynamic pattern. Right-heart filling pressures (central venous, right atrial and right ventricular end-diastolic pressures) are raised, while left ventricular filling pressures are normal or mildly raised. Right ventricular systolic and pulse pressures are low, and cardiac output is usually markedly depressed. In rare cases, this disproportionate elevation of right-sided filling pressure leads to right-to-left shunting through a patent foramen ovate. This possibility must be kept in mind in patients with right ventricular infarction with unexplained systemic hypoxemia. It is suggested that abnormally high levels of atrial naturetic peptide might in part be responsible for the hypotension seen in patients with right ventricular infarction due to the observed rise in atrial natriuretic factor in patients with this condition. Also, the protective effect of ischemic preconditioning described in cases of left ventricle infarction has also been reported in patients with right ventricle infarct. 28
ECG gives the first clue that right ventricular involvement is present in the patient with inferior STEMI .Most patients with right ventricular infarction have ST segment elevation in lead V4R (right precordial lead in V4 position).20 Transient elevation of the ST segment in any of the right precordial leads can occur with right ventricular MI, and the presence of ST segment elevation of 0.1 mV or more in any one or combination of leads V4R, V5R, and V6R in
patients with the clinical picture of acute MI is highly sensitive and specific for the diagnosis of right ventricular MI. Wellens emphasized that in addition to observing presence or absence of convex upward ST elevation in V4R, clinicians should determine whether the T wave is positive or negative-such difference helps to differentiate proximal from distal occlusion of the right coronary artery as well as from occlusion of the left circumflex artery 29 It is also observed that lead V1 faces RV and ST elevation in lead V1 is associated with increased mortality 30.
HERO 2 trial evaluated 7967 patients with inferior MI and found 25% increase in mortality for 0.5 mm ST elevation in lead VI.30 Elevation of the ST segments in leads V1 through V4 caused by right ventricular infarction can be confused with elevation caused by anteroseptal infarction, the ST segments are oriented to the right in right ventricular infarction (e.g., +120 degrees), whereas they are oriented to the left in anteroseptal infarction (e.g., -30 degrees).
ECHOCARDIOGRAPHY AND RADIONUCLIDE ANGIOGRAPHY.
Echocardiography is useful in the differential diagnosis distinguishing RV infarct from cardiac tamponade as in case of right ventricular infarction; little or no pericardial fluid accumulates in contrast to pericardial tamponade. The
echocardiogram shows abnormal regional wall motion of the right ventricle, as well as right ventricular dilation with depressed right ventricular ejection fraction.31 Magnetic resonance imaging also assists in diagnosing right ventricular infarction.32 Studies have shown that some degree of recovery of an initially depressed right ventricular ejection fraction is the rule with right ventricular infarction, to a greater degree than with left ventricular ejection fraction31
Many of the patients having normal left ventricular filling pressure and depressed cardiac index have right ventricular infarcts (with accompanying inferior wall infarcts). This hemodynamic picture may resemble that seen in patients having pericardial disease, that includes raised right ventricular filling pressure; steep, right atrial y descent; and an early diastolic drop and plateau (resembling the square root sign) in the right ventricular pressure tracing. Over and above, the Kussmaul sign (an increase in jugular venous pressure with inspiration) and pulsus paradoxus (a fall in systolic pressure of greater than 10 mm Hg with inspiration) may be present in patients with right ventricular infarction31 Kussmaul sign in presence of inferior STEMI is highly predictable for right ventricular involvement.
Loss of atrial support in right ventricular infarction causes marked decrease in stroke volume and arterial blood pressure. Disproportionate rise of the right-sided filling pressure is the hallmark of right ventricular infarction hemodynamically. Thus pacing of the ventricle may fail to increase cardiac output, and atrioventricular sequential pacing may be required.
Medications routinely used in left ventricular infarction may lead to profound hypotension in patients with right ventricular infarction, because of their tendency to reduce preload. 31 In patients presenting with hypotension due to right ventricular MI, hemodynamic can be improved by expanding plasma volume to augment right ventricular preload and cardiac output and arterial vasodilators when left ventricular failure is presen27
Initial management for hypotension in patients having right ventricular infarction should include volume expansion. When hypotension has not improved after 1 or more litres of fluid given briskly, further volume expansion may be of little value and may lead to pulmonary congestion therefore consideration should be given to hemodynamic monitoring with a pulmonary artery catheter. Vasodilators reduce the impedance to the left ventricular outflow and in turn left ventricular diastolic, left atrial and pulmonary (arterial)
pressures, thus decreasing the impedance to right ventricular outflow and increasing right ventricular output.
Right ventricular infarction commonly occurs among patients having inferior wall left ventricular infarction. Therefore unexplained systemic arterial hypotension and decreased cardiac output, or evidence of marked hypotension in consequence to small doses of nitroglycerin in inferior infarction, should lead to the consideration of this RV involvement. Due to the undoubted significance of atrial transport, patients requiring pacing should receive atrial or atrioventricular sequential pacing.22
Successful reperfusion of the right coronary artery markedly improves right ventricular mechanical function and reduces in-hospital fatality in patients with right ventricular infarction33
Tricuspid valve replacement and repair with annuloplasty rings has shown successful in the treatment of severe tricuspid regurgitation secondary to right ventricular infarction.
COMPLICATIONS OF INFERIOR MI
Shock and hypotension are frequently observed complications in inferior wall MI. Six patients (22.2 %) developed hypotension in a study carried out at Peshawar. 34
CONGESTIVE CARDIAC FAILURE
The absence of congestive heart failure was the best prognostic sign in MI patients. In a study it was found that patients who developed shock had 28 per cent mortality. 7.4% of patients presented with left ventricular failure in inferior MI in a study carried out at Peshawar 34
The SHOCK study observed early revascularization in treatment of patients with MI accompanied by cardiogenic shock. Long-term survival significantly improved in patients having cardiogenic shock who underwent early revascularization). 35 Thus early revascularization significantly influences the outcome of patients having concomitant cardiogenic shock.
Cardiogenic shock is considered to be the most severe clinical expression of left ventricular failure and is accompanied with extensive damage to the left ventricular myocardium in more than 80 percent of STEMI patients in whom it
occurs; the rest have a mechanical defect like ventricular septal rupture or papillary muscle rupture or right ventricular infarction. 36-37 In past, cardiogenic shock was reported to be in up to 20 percent of patients with STEMI, but recent estimates from large trials report an incidence rate in the range of 7 percent.42 Cardiogenic shock is the leading cause of death in about 60 percent of patients dying after fibrinolysis for STEMI. 35, 39
Older studies have documented that about thirty-seven percent of patients suffering cardiac arrest after complete heart block in myocardial infarction revived post resuscitation to return to normal life. Intracardiac pacing appeared to be of much significance in reducing mortality.
In a study, average in-hospital mortality rate estimated was 26% for women and 9% for men (p < 0.0005).Female patients (n = 257) were found to be significantly older and had a higher prevalence of diabetes and hypertension than males. A longer delay in seeking medical care was found in women (8 h vs. 6 h). Cardiogenic shock was also observed to be more frequent presentation among women than men.15
The incidence of CAVB complicating AMI is lower in the thrombolyticÂ era than in the prethrombolytic era. Mortality among patientsÂ having CAVB is still remains high and has not decreased over the lastÂ decade. The AMI patients with CAVB in the thrombolyticÂ era have much worse prognosis than those patients withoutÂ CAVB. Patients with peri infarction AV block have higher in-hospital and late mortality than do those with preserved AV conduction.9 Thus conduction disturbances have a grimmer prognosis, with a significant mortality rate even in the thrombolytic era.12, 41, 42 The increase in mortality risk is mainly observed within the first 30 days in case of both an inferior and an anterior myocardial infarction. However when acute myocardial infarction, is complicated by the AV block the long-term prognosis of survivors is mainly dependent on the extent of myocardial damage, the degree of heart failure, and incidence of hemodynamic complications.2,12, 42 In an Israeli study, During the 1990s, the incidence of CAVB was 3.7% compared withÂ 5.3% in the 1980s, p = 0.0007. In the 1990s, mortality of patientsÂ with CAVB was significantly higher than in those without CAVBÂ at 7 days (odds ratio [OR] = 4.05 95% CI [confidence interval]Â 2.34 to 6.82, 30 days OR = 3.98 [95% CI 2.44 to 6.43] and one-yearÂ hazard ratio [HR] = 2.36, [95% CI 1.68 to 3.30]) and similarÂ in thrombolysis-treated and not-treated patients. MortalityÂ of patients with CAVB has not much altered significantly betweenÂ the two eras; seven-day OR = 0.82 (95% CI 0.46 to 1.43);Â 30-day OR = 0.78 (95% CI 0.45 to 1.33) and one-year HR = 0.79Â (95% CI 0.54 to 1.56), respectively, in the 1990s as comparedÂ to a decade earlier.12
PRE HOSPITAL CARE.
The pre hospital care of patients having suspected STEMI is a substantial element in patient survival. Majority of deaths due to STEMI occur within the first 60 minutes of its onset. Thus, the overwhelming importance of the emergent institution of definitive resuscitative efforts and of rapid transport of the patient to a hospital cannot be overemphasized
Every patient being transported to hospital for evaluation of chest pain should be treated as if the pain were ischemic in origin unless concrete evidence to the contrary exists. Treating Physicians should heighten the awareness of patients at risk for STEMI (e.g., those with hypertension, diabetes, history of angina pectoris). They should reinforce with patients and their caretakers, the significance of seeking immediate medical attention for symptoms including chest discomfort, extreme fatigue, and dyspnoea, in particular if accompanied by diaphoresis, light-headedness, palpitations, or a sense of impending doom. 43, 44 Emphasis must be laid on the prevention and treatment of fatal arrhythmias, as well as saving the compromised myocardium by reperfusion, for which time is crucial element. Patients should be educated in the judicious use of sublingual nitroglycerin and to be able to call emergency services if the ischemic-type discomfort persists for more than 5 minutes 46
EMERGENCY MEDICAL SERVICES (EMS) SYSTEMS.
These have three major components:
1) Emergency medical dispatch,
2) First response, and
3) EMS ambulance response
Well-equipped ambulances and helicopters staffed by personnel trained adequately in the acute care of the STEMI patient allows definitive therapy to initiate before the patient is transported to the hospital. These units must be equipped with monitoring equipment that are battery-operated, a DC defibrillator, oxygen supply , endotracheal intubation kit and suction apparatus, and commonly used cardiovascular drugs. Radiotelemetry systems are highly desirable to facilitate triage of STEMI patients and are becoming increasingly available in many communities
Pre hospital notification should alert the ED staff to the possibility of an AMI by Emergency Medical Personnel
Specific pre hospital care includes:
IV access with supplemental oxygen and saturation monitoring using pulse oximetry
Administration of aspirin and sublingual nitro glycerine
Several randomized trials have been conducted to evaluate the potential benefits of prehospital as compared to in-hospital fibrinolysis. Although a significant reduction in mortality with prehospital-initiated thrombolytic therapy was documented by none of the individual trials, there was a general observation of benefit from earlier treatment, and a meta-analysis of all trials available showed a 17 percent reduction in mortality.47
The CAPTIM trial reported a lower rate of mortality among STEMI patients having prehospital fibrinolysis when compared with primary PCI patients, especially if patients received treatment within 2 hours of the symptoms onset. 48-49 Several other reports provide further support for the benefit of prehospital fibrinolysis. 50-51
GENERAL TREATMENT MEASURES
This agent is a part of the early management plan in STEMI patients. Aspirin halts formation of thromboxane A2 in platelets (which is a potent activator of platelets) by cyclooxygenase inhibition. Since low doses of aspirin(40 to 80 mg) would take several days for its complete antiplatelet effect, at least a dose of 162 to 325 mg must be administered immediately in the emergency department.27 Early administration of aspirin reduces the 35 day mortality rate by 23% as compared to a placebo.
CONTROLLING CARDIAC PAIN.
Relieving pain is a key element in treating of STEMI.
Cardiac pain is mainly relieved with simultaneous use of analgesics (e.g., morphine), nitrates, oxygen, and beta blockers.
Although varieties of analgesics have been employed to treat pain due to STEMI, morphine is the drug of choice.
Four to 8 mg of morphine are usually administered intravenously, and 2 to 8 mg are repeated at 5 to 15 minutes interval until the pain subsides or side effects including hypotension, respiratory depression or vomiting appears precluding more administration of this drug. Some patients require large cumulative morphine doses (2 to 3 mg/kg) and are usually tolerated well.
It reduces anxiety and thus decreases the patient's restlessness and the sympathetic over activity of the autonomic nervous system, with a resultant decline of the heart's metabolic demands. The useful influence of morphine in patients developing pulmonary oedema can not be ignored and is related to multiple factors that include peripheral arterial and venous dilation (especially in patients having excessive sympathoadrenal drive), slowing the
work of breathing, and reducing the heart rate in addition to withdrawal of sympathetic and augmenting of vagal tone
Nitrates have the ability to increase coronary blood flow through coronary vasodilatation and to reducing ventricular preload through enhancement of venous capacitance. Sublingual nitrates are given to patients presenting with acute coronary syndrome. However, patients with inferior MI and concomitant right ventricular infarction should not receive sublingual nitroglycerin 52 as well as those having marked hypotension (with systolic pressure <90 mm Hg), especially when accompanied with bradycardia.
Once it is determined that hypotension is absent, sublingual nitroglycerin must be administered and the patient should be observed for symptom improvement or change in hemodynamic status. If dose is well tolerated initially and appears to be beneficial, further nitrates can be given, while monitoring the vital signs. It must be remembered that even small doses of nitro glycerine can cause sudden hypotension along with bradycardia, which can be life-threatening but commonly easily reversible with intravenous atropine if early recognized. Oral nitrate preparations that have longer duration of action must not be used early in the course of STEMI due to the frequently altering hemodynamics of the patient. Intravenous nitroglycerin is of benefit in alleviating symptoms as well as correcting ischemia in patients having prolonged episodes of chest pain, however frequent blood pressure monitoring is required.
These drugs reduce pain, decrease the requirement for analgesics in many patients, and also decrease the infarct size as well as life-threatening arrhythmias. Withholding early intravenous beta blockade in case of patients having Killip Class II or greater is important, due to the risk of precipitating into cardiogenic shock. 54-55
A relatively safe protocol for the judicious use of a beta blocker is as follows.
(1)Patients having heart failure (with rales >10 cm up from diaphragm), hypotension (having blood pressure <90 mm Hg), bradycardia (with heart rate <60 beats/min), or heart block (with PR interval >0.24 sec) are first excluded from receiving beta blockers.
(2) Metoprolol may be given in boluses of three 5-mg intravenous each, patients are observed for 2 to 5 minutes after giving each bolus, and if the heart rate drops less than 60 beats/min or systolic blood pressure drops below 100 mm Hg, further drug should not be given.
(3) If patient remains hemodynamically stable for at least 15 minutes after the last intravenous bolus, the patient may be started on oral metoprolol, 50 mg tablet every 6 hours for 48 hours, then switched to 100 mg twice daily dose. An infusion of esmolol (50 to 250 mg/kg/min), that is extremely short-acting beta blocker, can be beneficial in patients with relative but not absolute contraindications to beta blockade in whom heart rate slowing is considerably desirable.
Ventilation-perfusion abnormalities as a consequence to left ventricular failure may result in hypoxemia in patients having STEMI; Pneumonia and intrinsic lung disease are additional reasons of hypoxemia. All patients with STEMI who are hospitalized with should be treated with oxygen for at least 24 to 48 hours, due to the evidence that increased fractional inspired oxygen may be protective for ischemic myocardium. However, this practice is expensive. On the other hand, it causes an increase in systemic vascular resistance and arterial pressure and thus slightly decreasing cardiac output.
In view of above reasons, Blood oxygen saturation can be checked by pulse oximetry (which is an easily available), and oxygen therapy can be withheld if normal pulse oximetry. On the other hand, oxygen should be given to patients with STEMI when hypoxemia is present clinically 27 In case of these patients, serial arterial saturation measurements and blood gas analysis can be of use to monitor the adequacy of oxygen therapy. The administration of 2 to 4 litres/min of 100 percent oxygen by means of face mask or via nasal prongs for 6 to 12 hours is adequate for most patients having mild hypoxemia. But if arterial oxygenation saturation is still low, the flow rate of oxygen will have to be increased, and clinician will have to seek other causes for hypoxemia. In case of patients with pulmonary oedema, positive-pressure controlled ventilation and endotracheal intubation may be necessary.
Fibrinolytic therapy is reported to reduce short term in hospital mortality in patients with inferior MI.55 Although late spontaneous re-perfusion is reported in some patients, thrombotic occlusion usually persists for most of patients with STEMI.56 Timely reperfusion and restoring blood supply to jeopardized myocardium is the most effective way of re-establishing the balance between the oxygen supply of heart and its demand.56 When thrombolytic therapy is administered the extent of myocardial protection is shown to be directly related to the avidity with which reperfusion is employed after coronary occlusion.56 Evidence suggests that the myocardial salvage after reperfusion with PCI (including stent deployment) is less dependent on time than that for fibrinolysis.57 The mechanisms underlying this therapy-related influence of time-to-therapy on myocardial salvage although not well understood but may include restoration of antegrade blood flow in the infarct related artery with PCI and reduced efficacy of other fibrinolytic agents due to maturation of coronary thrombi with the passage of time.58 A statistically significant increase in mortality has been shown with increasing delays between the symptom onset and PCI. 57, 59 Each 30-minute delay in PCI from symptom onset increases by the relative risk (RR) of 1-year mortality by 8 percent.60
The Fibrinolytic Therapy Trialists' Collaborative Group (FTT) compiled an overview of nine trials over thrombolytic therapy, each enrolling more than 1000 patients, 52 the database overview consisted of 58,600 patients in total including 6177 patients (10.5 percent) who died, 564 patients (1 percent) experienced a stroke, and 436 of the patients (0.7 percent) had major bleeds(non cerebral).. The results indicated an overall 18 percent decrease in short-term mortality, and 25 percent decline in mortality among 45,000 patients having ST segment elevation or bundle branch block., LATE and EMERAS ,trials show that a mortality reduction may be observed among patients given treatment with thrombolytic agents in 6 and 12 hours from the of symptom onset . Data from LATE and EMERAS as well as FTT overview provide the evidence and support for extending the treatment window with thrombolytic agents up to 12 hours from the symptom onset.
A study carried out in Spain including a total of 449 patients showed a reduced incidence of AV blocks with fibrinolysis 38% of those having thrombolysis as compared to 61 % in those without fibrinolysis. Duration of AV block was also much reduced in patients with thrombolysis. The mean duration of block being 75 minutes in those with thrombolysis and 24 hours in patients without thrombolysis.61
TISSUE PLASMINOGEN ACTIVATOR
The administration of t-PA over 90 minutes produces a rapid thrombolysis than 3-hour standard infusion of t-PA. Recommended dosage for t-PA is a 15-mg intravenous bolus given initially, followed by infusion of 0.75 mg/kg over 30 minutes (maximum 50 mg, followed by infusion of 0.5 mg/kg over 60 minutes. (Maximum 35 mg)
This is recombinant form of t-PA
The GUSTO III trial evaluated the comparison between the reteplase and accelerated t-PA in about 15,059 patients.63 The results of the trial exhibited no superiority of the reteplase over that of t-PA therapy.64-66 .Although the GUSTO III trial did not completely fulfil the criteria of equivalence between reteplase and t-PA, however many of the clinicians still consider the two agents to be similar therapeutically and think of the double-bolus method of giving reteplase to have superiority over t-PA.
Tenecteplase is mutant of t-PA having specific substitutions of amino acid in kringle 1 domain as well as protease domain which is introduced to decrease its plasma clearance and increase fibrin specificity, and also to reduce its sensitivity to the plasminogen activator inhibitor-1 A dose of 0.53 mg/kg is considered to be optimal for sustaining high rates of TIMI grade 3 flow.74. Safety of tenecteplase was considered in both TIMI 10B and ASSENT 1 trial,
large phase II clinical trial.68-70 In ASSENT 2 trial tenecteplase or t-PA did not show much difference in efficacy in any specific subgroup of patients, with the exception of those patients who were treated after 4 hours from symptom onset , among these patients the mortality rate was observed to be 7.0 percent with tenecteplase and 9.2 percent mortality with t-PA (p = 0.018). 69.
OTHER FIBRINOLYTIC AGENTS.
Urokinase is used rarely as an intracoronary infusion (6000 IU/min) to a cumulative dose of 5,000,000 IU in order to lyse intracoronary thrombi that are thought to be responsible for evolving STEMI.
Is given in a dose of 30 mg over 2 to 5 minutes through intravenous route .Its , side-effect profile is similar to streptokinase, and its potency profile is similar to conventional-dose t-PA, while its mortality benefit is similar to that of either streptokinase or t-PA . For the lack of any significant advantages apart from its bolus administration and higher costs, anistreplase is not a very frequently prescribed drug for STEMI.
Is a fibrin-specific plasminogen activator which requires priming on surface of the clot? A pegylated, recombinant form of this drug has shown to provide TIMI grade 3 flow rates that are similar to those achieved with t-PA.70
ARYTHMIAS IN MI
The main abnormalities of conduction accompanied with acute MI include AV blocks as well as intraventricular conduction disturbances9, 12.
They result from autonomic imbalance as well as ischemia and necrosis of the conduction apparatus. In spite of the finding the newer ways for the treatment of acute myocardial infarction (which include percutaneous coronary intervention and thrombolysis), incidence of the intraventricular conduction disturbances has not signiï¬cantly altered, although the frequency of AV blocks has declined but remains quite high still. 9, 12, 40
An Israeli study showed an incidence of CAVB of about (6.0%) among patients having inferior wall myocardial infarction 21
In TIMI study the incidence of CAVB was observed to be 12% as compared to 20 % incidence pre thrombotic era.
Anatomy and Blood Supply of the Conduction SystemÂ -
Understanding the anatomy as well as blood supply of the conduction system is essential before further discussion can be made as to the conduction abnormalities accompanying acute myocardial infarction.
Once the bundle of His leaves the AV node it bifurcates into the right and left bundle branches at junction of the boundaries (fibrous and muscular) of inter ventricular septum .Right bundle branch courses downwards on the right side of inter ventricular septum close to the endocardium in the upper third of its course , it than passes deeper in the middle third of its course into the muscular portion of inter ventricular septum, and then in lower third of its passage it again passes near the endocardium Right bundle branch does not divide through major portion of its course, however it starts to branch as it comes close to the base of right anterior papillary muscle with its fascicles passing to the septal as well as the free wall of the right ventricle.
Main left bundle branch enters the interventricular septum's membranous portion by passing under the aortic ring.
After short course, it bifurcates into two or three separate branches, an anterior fascicle (a predivisional segment) passes across the left ventricular outflow tract; it ends up in anterolateral wall of left ventricle, in the Purkinje system. A posterior fascicle spreads inferiorly and posteriorly. In 65 percent of hearts, a fascicle passes to the interventricular septum.
Blood SupplyÂ -
An insight into the blood supply of the different parts of the conduction system is essential for understanding the relationship between dysrhythmia and myocardial infarction 19
SA node -
Its blood supply in 60 percent of patients is by the right coronary artery (RCA); and in rest 40 percent case its by the left circumflex artery (LCX)
AV node -
In 90 percent of cases it receives its blood supply by the RCA (AV nodal branch) and in rest of 10 percent cases it is through the LCX
His bundle -
It receives its supply by the RCA (AV nodal branch) with a small contribution of the left anterior descending artery (LAD) through the septal perforators
Main or proximal left bundle branch -
Left bundle branch receives most of the blood supply from the LAD coronary artery especially for its initial portion. It also receives some collateral flow through the RCA and LCX systems
Left posterior fascicle -
AV nodal artery supplies blood flow to the proximal part of the left posterior fascicle but at times it may be supplied by septal branches of LAD. The distal
portion of left posterior fascicle has a double blood supply receiving from both anterior as well as posterior septal perforating arteries
Left anterior fascicle -
The left anterior fascicle as well as mid-septal fascicles receive blood supply through the septal perforators of LAD .In one-half of cases they receive supply by AV nodal artery.
Right bundle branch -
Most of the blood supply of the right bundle branch is from septal perforators arising from the LAD coronary artery, especially early in its path. RCA or LCX coronary systems also provide some collateral supply, depending on which system is dominant.
The arrhythmias after acute MI of the inferior wall are more frequent when the coronary trunk is occluded at or near its origin. This is because of the presence of right superior descending artery, given off by right coronary trunk about 1 centimetre from the origin. The arrhythmias due to the left circumflex artery occlusion are due to the presence of Kugel's artery, 71
TYPES OF BRADYARYTHMIAS IN MI
Defined as heart rate less than 60/min with SA node as the prime pacemaker.71
Atrioventricular and Intraventricular Block
Definition-Â Atrioventricular (AV) block may be defined as a delay or interruption in transmission of impulse from the atria to the ventricles as a result of an anatomical or functional impairment in conduction system. The conduction disturbance may be transient or permanent.
First-Degree Av Block, orÂ PR Prolongation,
It is disease ofÂ conduction systemÂ of the heart Â in which there is lengthening of PR interval more than 0.20 seconds 27
In case of first-degree AV block, the electric impulse conduction from atria to the ventricles through AV node is deferred and travels much slower than usual.Â In the normal adult population, it has aÂ prevalence of 0.65-1.1%, with the incidence Â of 0.13 per 1000 persons.
No symptoms or signs are associated with isolated first degree AV block. It is thought of as having a benign course. However, theÂ Framingham Heart Study it was noted that, the presence of a first degree AV block doubled the risk of atrial fibrillation, tripled the risk of need for anÂ artificial pacemaker, and it was also accompanied with a slight increase in mortality. This risk being proportional to degree of PR prolongation.13
Third Degree AV BlockÂ -Â
In case of third degree AV block atrial impulses fails to reach the ventricle. The block may exist in AV node or it may originate in the infranodal conduction system. 72
Atrioventricular block is reported at the three different levels: at AV nodal level (16 to 25%), at intra-His bundle (14 to 20%), and at infra-His bundle level (56 to 68%)Â 72
An electrocardiographic study of His-bundle may elaborate the site of block with precision, but the evidence of the escape rhythm also gives significant clues.
Escape RhythmsÂ -
Â Escape rhythms usually occur when pacemaker other than the sinus node attains the threshold, and produce a depolarization. In case of complete heart block, the escape rhythm controlling the ventricles can arise at any level below the level of conduction block and QRS complex morphology can assist in determining the location of the block.
If the third degree block originates in the AV node, then two-thirds of escape rhythms will have narrow QRS complexes that are either junctional rhythm or AV nodal rhythm. Blocks occurring at the level of His bundle, are also commonly accompanied with a narrow QRS complex morphology. Patients developing a trifascicular heart block have a wide QRS complex
Thus in escape rhythm having a normal QRS duration of less than 120 msec, then the block occur with near equal frequency in both the AV node and the His bundle. On the contrary, these sites are infrequently involved in case of prolonged QRS complexes, the block in this condition is either in the fascicles or located in the bundle branches in more than 80 percent cases
CONDUCTION DISTURBANCES AND INFARCT LOCATIONÂ -Â
The type of conduction abnormality that occur in myocardial infarction is influenced by the infarct location 2, 9, 12 ,40-42
AV block that occur in setting inferior wall infarction are localized above the bundle of HIS in the majority of the patients, while in case of anterior wall infarctions, AV blocks are more commonly present below AV node.
High degree AV block that occur with inferior wall MI is mostly located aboveÂ the bundle of HIS in 90 percent of cases.19, 24 Therefore, complete heart block is usually accompanied with a transient bradycardia and junctional escape rhythm with heart rates more than 40 beats per minute. Junctional pacemaker can often control the ventricles to a heart rate above 60 beats/min. The QRS complexes are narrow in this situation and are accompanied with a low rate of mortality
Blocks associated with anterior wall MI have an unstable, escape rhythm with wide QRS complexes and excessively high mortality reaching up to 80% due to the severe necrosis of the myocardium.17 Intraventricular conduction abnormalities develop more frequently in the case of an anterior-anteroseptal infarction due to its speciï¬c blood supply. The presence of conduction abnormalities in the course of acute myocardial infarction is has an unfavourable prognosis and leads to an increased chance of sudden cardiac death (SCD).
MECHANISM OF ARRHYTHMIA.
Major mechanism of arrhythmias in the early course of coronary occlusion is thought to be due to re-entry as a result of in homogeneity of electrical characteristics of the ischemic heart tissue.73
The electrophysiological mechanisms at cellular level in case of reperfusion arrhythmias seems to involve washout of ions such as lactate as well as potassium along with toxic metabolic substances accumulating in ischemic zone.
Patients who have substantial dysfunction of left ventricle have more or less a fixed stroke volume which relies on alterations in heart rate to change cardiac output. However, the range of heart rate over which the cardiac output is maximal is narrow, with drastic decline occurring at both fast and slow heart rates.
Thus it is observed that in STEMI, cardiac output can be depressed by all sorts of bradycardia and tachycardia. Although the optimal rate insofar as cardiac output is concerned may exceed 100 beats/min, it is important to consider that heart rate is one of the major determinants of myocardial oxygen
consumption and that at more rapid heart rates, myocardial energy needs can be elevated to levels that adversely affect ischemic myocardium. Therefore in patients with STEMI, the optimal rate is usually lower, in the range of 60 to 80 beats/min.
A second factor to consider in assessing the hemodynamic consequences of a particular arrhythmia is the loss of the atrial contribution to ventricular preload.
Studies in patients without STEMI have demonstrated that loss of atrial transport decreases left ventricular output by 15 to 20 percent. In patients with reduced diastolic left ventricular compliance of any cause (including STEMI), however, atrial systole is of greater importance for left ventricular filling.
In patients with STEMI, atrial systole boosts end-diastolic volume by 15 percent, end-diastolic pressure by 29 percent and stroke volume by 35 percent.
BRADY ARYTHMIAS IN INFERIOR MI
Â Conduction disturbance in inferior MI can occur acutely or may occur after hours or even days. Sinus bradycardia, Mobitz type I, and complete AV blocks are usually seen, as the SA node, the AV node, and bundle of HIS receive their main supply from the RCA 24
About 40 percent AV blocks are due to Ischemic heart disease. Conduction disturbance may occur during either an acute myocardial infarction (MI) or with chronic ischemic heart disease. It is observed that about 20 percent of patients presenting with an acute MI may develop AV block: first degree being present in 8 percent; with second degree AV block in 5 percent; and third degree AV block in about 6 percent of patients 74
Intraventricular conduction delays (IVCDs), that include bundle branch blocks and fascicular blocks, are reported in 10 to 20 percent of acute MI patients. Right bundle branch block and left bundle branch block occurring with left anterior hemi block are most frequent, each of them occurring in one-third of cases having IVCD 13 RBBB occurring either with or without left posterior fascicular block as well as alternating bundle branch block is seen less frequently also isolated left fascicle block (either anterior or posterior fascicle block) are quite uncommon.
Sinus bradycardia -
Sinus bradycardia occurs commonly during the early phases of STEMI, particularly in patients with inferior and posterior infarction.27
The most common arrhythmia accompanied with inferior MI is sinus bradycardia. It occurs in about 40 percent of cases as soon as the first two hours, and declining to about 20 percent at 24 hours. In a study carried out at Peshawar Sinus Bradycardia occurred in (29.6%) of inferior MI patients 34
Increased vagal tone is responsible for 1st degree AV blocks in first 24 hours after myocardial infarction. Transient sinus node dysfunction occurring later may be due to sinus node or atrial ischemia On the basis of data obtained in experimental infarction and from some clinical observations, the increased vagal tone that produces sinus bradycardia during the early phase of STEMI may actually be protective, perhaps because it reduces myocardial oxygen demands. Thus the acute mortality rate appears similar in patients with sinus bradycardia as in those without this arrhythmia.
Isolated sinus bradycardia, without evidence of ectopic beats or hypotension is observed rather than treated initially. In the first 4 to 6 hours after infarction, if the sinus rate is extremely slow (<40 to 50 beats/min) and associated with hypotension, intravenous atropine in doses of 0.3 to 0.6 mg every 3 to 10 minutes (with a total dose not exceeding 2 mg) can be administered to bring the heart rate up to approximately 60 beats/min.
FIRST DEGREE AV BLOCK-
First degree AV block is characterized by PR interval prolongation. It arises either in AV node, the f His bundle, or it may originate in the bundle branches.
Ist degree block at the level of the AV node is common after RCA occlusion which usually gives origin to AV nodal artery as well as the blood vessels to the posterior and inferior wall of the myocardium.
First degree AV block due to occlusion of RCA is usually due to AV nodal ischemia, occurring as a consequence of increased acetylcholine release from the postero-inferior wall of heart, or may occur by rendering AV node hypersensitive to acetylcholine IST degree block as a result of RCA occlusion with the AV nodal involvement is mostly brief in duration, it commonly resolves in a weak and requires no therapy. In the 10 percent of individuals
LCX t supplies the AV node and its occlusion may have direct affect on AV node. In small percentage of cases, first degree AV block occurs belowÂ the AV nodal level in patients with anterior MI, a condition expected if first degree heart block occurs in setting of a widened QRS complex.
IST degree AV block has no significant hemodynamic impact in course of inferior MI and does not require treatment. Beta blocking agents and calcium channel blockers (apart from nifedipine) lead to AV conduction prolongation and may cause first-degree heart block as well. But, discontinuation of both beta blockers and calcium channel blockers in STEMI can tend to increase ischemia as well as ischemic injury. The clinical practice is therefore to continue the usual dosage of these useful drugs until PR interval is exceeds 0.24 second and these agents be stopped only if patient is hemodynamically unstable or higher degree AV blocks are present.
If block that occurs in association with hypotension and sinus bradycardia as a result of excessive vagal tone ,then of atropine administration can be of use.
Continued monitoring of ECG rhythm is important in these patients due the possibility of their progression to higher degrees of block.
HIGH DEGREE AV BLOCK
Data from 75 993 patients enrolled in four large, randomized, clinical trials (GUSTO-I, GUSTO-IIb, GUSTO-III,