Manual of Medical Emergencies PG Raman, LC Gupta
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1Emergency Conditions
2

Acute Myocardial InfarctionChapter 1

 
INTRODUCTION
Myocardial infarction is a medical emergency caused by occlusive coronary thrombus in most patients. Mortality from AMI is greatest within the first 2 hrs (> 50% of all AMI deaths) after the onset of symptoms and can be significantly reduced by rapid transport to the hospital and institution of prompt management.
 
PATHOPHYSIOLOGY
AMI occurs when coronary plaques (with a rich lipid core and a thin fibrous) cap rupture and a mural thrombus forms at the site of rupture and leads to coronary artery occlusion. Whereas slowly developing high grade stenosis of epidcardial coronaries may progress to complete occlusion but do not usually precipitate AMI, probably because of the development of a rich collateral network.
 
Non-atherogenic Causes of AMI
1. Arteritis and collagen vascular disease. 2. Trauma to coronary art vcxxeries. 3. Spasm of coronary artery—Prinz metal's angina, after morphine withdrawal. 4. Embolic from infective endocarditis, MVP, cardiac myxoma. 5. Congenital anomalies of coronary artery. 6. Myocardial oxygen demand and supply disproportion—aortic stenosis, aortic incompetence, thyrotoxicosis.
 
CLINICAL PRESENTATION (TABLE 1.1)
  1. Most AMI occurs in between 6 AM to 12 noon (due to a combination of an increase in sympathetic tone and an increased tendency to thrombosis between this time period)
  2. Pain is the most common presenting complaint:
    1. It is deep or visceral; typically heavy, squeezing and crushing or stabbing and burning.
    2. It resembles that of angina but usually more severe and lasts longer (>30 min).
    3. It involves the central portion of the chest and/or epigastrium and may radiate to the arms, back, lower jaw, neck, abdomen but never below the umbilicus.
    4. The pain is often accompanied by weakness, sweating, nausea, vomiting, anxiety and with sense of impending doom.
  3. Silent MI
    1. Usually associated with diabetes mellitus, hypertension and old age.
    2. Between 20 and 60% of non-fatal MIs are unrecognized by the patient and (are discovered only on routine ECG or postmortem examination. Of these patients, 50% are truly silent.
  4. Physical findings
    1. Most patients are anxious and restless, moving about in bed. Pallor associated with perspiration and coolness of the extremities occurs commonly.
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      Table 1.1   Effort angina/acute myocardial infarction
      Points
      Effort angina
      A cute myocardial infarction
      A. History
      1. Cardiac Pain:
        1. Precipitating
        2. Severity
        3. Duration
        4. Releived by
      2. Dyspnoea
      3. Symptoms of shock cold extremities, excess sweating, oliguria, etc.
      4. Fever
      5. Recurrent attacks of pain in the past.
      Exercise, emotional upset, etc. but it never occurs at rest.
      Severe 1/2 to 3 min. Rest or nitroglycerine tab
      Absent
      Absent
      Present
      It may occur at rest without any provocation or may be opted by some factors.
      Very severe.
      Many hours.
      Only by deep sedation.
      Present
      Present 24–48 hours after the attack.
      Absent
      B. Physical Examination
      1. Attitude of the patient during attack
      2. Orthopnoea
      3. Cyanosis
      4. Pulse
      5. BP
      6. Examination of heart
      7. Examination of lung
      8. Emboli
      Investigations
      • ECG
      1. Leucocyte
      2. SGOT & SGPT level CPK level
      Motionless
      Absent
      Absent
      Normal
      Normal or slightly
      elevated.
      Normal or evidence of underlying factors present.
      Normal
      Absent
      Depression of ST segment and inversion of T wave
      Absent
      Normal
      Restless, tossing over the bed for relief of pain
      Present
      Present
      Arrhythmias, pulses alternans, extremely low vol. pulse due to shock present
      Falls
      Cardiac enlargement gallop rhythm, soft systolic murmur, pericardial rub, etc. present.
      Basal crepitation present Present
      Elevation or ST segment, depression T wave and presence of abnormal Q wave
      Present
      Elevated
    2. About 1/4th of patients with anterior infarction have manifestation of sympathetic activity (tachycardia and/or hypertension) and upto one half with inferior infarction show evidence of parasympathetic hyperactivity (bradycardia and/or hypotension)
    3. The precordium is usually quiet and the apical impulse may be difficult to palpate.
    4. S4, S3, decreased intensity of heart sounds, paradoxical splitting of S2, transient apical systolic murmur, pericardial friction rub may be found and should be looked for.
  5. Atypical presentations:
    1. CHF.
    2. Classical angina pectoris without a particularly severe or prolonged attack.
    3. Atypical location of the pain.
    4. CNS manifestation like stroke, unconsciousness, confusion.
    5. Apprehension and nervousness.
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      Table 1.2   Differential diagnosis of AMI patients
      S. Diagnosis No.
      ECG findings mimicking MI
      Diagnostic evaluation
      1. Pericarditis
      ST elevation
      Echocardiography
      2. Myocarditis
      ST elevation, Q waves
      Echocardiography
      3. Acute aortic dissection
      ST elevation or depression, non-specific ST & T changes
      Transesophageal echo, chest CT or MRI aortography
      4. Pneumothorax
      New poor R wave progression in lead V1-V6, acute QRS axis shift.
      Chest X-ray
      5. Pulmonary embolism
      Inferior ST elevation, ST shifts in leads V1-V3
      Ventilation /perfusion scan.
      6. Acute cholecystitis
      Inferior elevation
      ST Gallbladder USG or radio isotope scan.
    6. Sudden mania or psychosis.
    7. Syncope.
    8. Severe weakness.
    9. Acute indigestion.
    10. Peripheral embolism.
    11. Unexplained drop in arterial pressure.
  6. Differential diagnosis (Table 1.2)
  7. Laboratory diagnosis
    1. Electrocardiogram
      1. ST-T changes—convex ST segment elevation (> 1 mm) in at least two contiguous leads with either peaked upright or inverted T-waves usually is indicative of acute myocardial injury, the early stage of a transmural Q wave MI. ST segment depression (> 1 mm) particularly when it persists (> 12 hours), may also be indicative of a non-Q wave MI.
      2. Q waves—the development of new Q waves (> 40 msec.) is generally diagnostic of MI but may occur in patients with prolonged ischemia and occasionally, in patients with myocarditis.
    2. Cardiac enzymes (Table 1.3)
    3. Serum lipids A lipid profile should be obtained on all AMI patients within 24 to 48 hrs of symptoms. If delayed, it is best to defer determinations of serum lipid levels until at least 8 weeks after the infarction has occurred.
    4. Hematological manifestations Polymorphonuclear leucocytosis, which develops in 2 hrs after the onset of chest pain, persists for 2 to 7 days and may reach up to the levels of 12,000 to 15,000/ml.
      Table 1.3   Several cardiac enzymes
      S. No
      Marker
      Range of times to initial elevation (h)
      Mean time to peak elevation (non-thrombolysis)
      Time to return to normal range
      Most common sampling schedule
      1.
      CTnI
      3–12
      24 hrs
      5–10 days
      Once at least 12 hrs after CP*
      2.
      CTnT**
      3–12
      12h - 12 day
      5–14 days
      Once at least 12 hrs after CP
      3.
      MB-CK***
      3–12
      24 hrs
      48–72 hrs
      Every 12 hrs × 3
      4.
      Myoglobin
      1–4
      6–7 hrs
      24 hrs CP
      Frequent; 1–2 hrs after
      5.
      LDH
      10
      24–48 hrs
      10–14 days after CP
      Once at least 24 hrs
      6.
      Enolase
      6–10
      24 hrs
      48 hrs
      Every 12 hrs × 3
      *Clinical presentation;
      **Cardiac specific troponin-T (CTnT) and troponin-I (CTnI) - Since CTnT and CTnI are not normally detectable in blood of healthy individuals, but may increase after myocardial infarction to levels over 20 times higher than the cutoff value, measurement of CTnT or CTnI is of considerable diagnostic value.
      ***Creatinine phosophokinase (CK). An important drawback of total CK measurement is its lack of specificity for MI. The MB isoenzyme of CK has the advantage over total CK that it is not present in significant concentration in extracardiac tissue and therefore is considered more specific. However, cardiac surgery, myocarditis and electric cardioversion often result in elevated levels of the MB isoenzyme.
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      The ESR raises more slowly, peaks during the first week and sometimes remaining elevated for 1 to 2 weeks.
    5. Cardiac imaging
      1. Two dimensional echocardiography is indicated in patients with refractory ischemic chest pain and a non-diagnostic ECG to detect regional wall motion abnormalities.
      2. 99mTc pyrophosphate scintigraphy is rarely used to diagnose MI. The technique is highly sensitive (> 90%) for detecting large transmural infarct but is less reliable in detecting small, non-Q wave MIs.
      3. Myocardial perfusion imaging with 201Thalium or 99mTc will demonstrate perfusion defects within the first 6 hours of MI.
      4. Radionuclide ventriculography allows for characterization of right and left ventricular ejection fraction (EF) and assessment of regional wall motion abnormalities.
      5. Coronary angiography and left ventriculography are rarely indicated to exclude coronary occlusion and wall motion abnormalities in patients with refractory chest pain and non-diagnostic ECG changes (Table 1.4).
 
MANAGEMENT
 
Initial Management
  1. Rapid triage to reperfusion therapy.
    zoom view
    Table 1.4   Episodic thoracic pain
    Angina pectoris
    Substernal visceral discomfort or distress, provoked by effort, emotion, eating, and, occasionally by lying down. Relieved by restand nitroglycerin.
    Pleural pain
    Precipitated by breathing or coughing usually described as sharp. Associated physical and radiographic findings of pleurisy
    Pain of pulmonary
    Not closely related to activity or relieved by rest.
    Hypertension
    Associated signs and symptoms of pulmonary hypertension and pulmonary disease
    Esophageal pain
    Burning and substernal, with occasional radiation to the shoulder. Nocturnal occurrence (when lying flat). Relief with food or antacids
    Peptic ulcer
    Nearly always intradiaphragmatic and epigastric. Nocturnal occurrence and daytime attacks relieved by food. Not worsened by activity
    Biliary disease
    Usually under right scapula, prolonged in duration. Biliary disease is more important as triggering mechanism for angina than as a mimic
    Cervical disc
    History of injury is common; provoked by activity only insofar as neck movement is involved. Persists after activity is discontinued. Local palpation and movement may produce pain
    Arthritis-bursitis
    Usually of long (hours) duration. Local tenderness of pain with movement
    Neurocirculatory (Vaso-regulatory asthenia)
    Prolonged aches in various asthenia chest locations (often with arm radiation) likely to come at the end of an active day. Lethargy and fatigue, sighing respiration
    Hyperventilation
    Tingling in circumoral area or hands anxiety. Usually marked complaints of breathlessness without evidence of lung disease.
    Chest wall (Musculoskeletal)
    Provoked by movement, especially twisting, bending, etc. Usually longlasting and often associated with local tenderness
    Psychoneurosis
    Virtually always after anxiety, poorly described complaints, intramammary location of pain.
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  2. Initial Treatment in All Patients
    1. Antiplatelet therapy. All patients should be given 160–325 mg of soluble aspirin by mouth, preferably chewed to enhance absorption.
    2. Nitrate
      • Predominant venodilator, reduce preload.
      • Should be given to all patients with ischemic chest pain in the absence of systolic BP < 90 mmHg, marked sinus tachycardia (> 110/hr.), excessive bradycardia (< 50/min.) or inferior MI complicated by right ventricular infarction.
      • Up to 3 doses of 0.4 mg sublingually should be administered at about 5-min intervals. If symptom persists, morphine should be given.
      • Use IV nitrate's for 24–48 hours in patients with transmural anterior wall acute MI with ongoing anginal pain, with CHF or severe hypertension. Initiate dose—5–10 μg/min until mean BP is reduced by 10% of its baseline level in normotensive and by 30% for hypertension.
    3. Morphine
      • The analgesic of choice for the treatment of chest pain of MI.
      • It induces modest venodilatation, which decreases preload, has a modest arterial vasodilating effect, and has a vagotonic effect that can decrease heart rate.
      • Dose is 4 mg IV, which can be repeated every 5–10 min until pain is controlled or side effects develop. Nausea or vomiting can be treated with an antiemetic agent. Hypotension is prevented by adequate volume expansion and the vagotonic effects of morphine can be treated with 0.5 mg IV atropine.
    4. Anticoagulation with heparin should be initiated with a bolus of 70–80 U/kg (5000 U) followed by infusion of 15–18 U/kg/hr (1000 U/hr).
    5. Beta blockers
      • Reduce myocardial ischemia and may limit infarct size (when used ≤ 4 hours from chest pain) and reduce chances of ventricular arrhythmias.
      • Should be given to all patients in the absence of (1) CHF; (2) HR< 60/min.; (3) Systolic BP < 90 mmHg; (4) PR interval > 0.24 sec; (5) Advanced heart block; (6) COPD; (7) Peripheral vascular disease.
      • Therapy may be initiated with an IV bolus of metoprolol 5 mg; can be repeated every 5 min to a total of 15 mg followed by oral metoprolol 50 mg, q. 6–12 hours and then to 100 mg BD (or atenolol 100 mg PO q.d.).
    6. Oxygen therapy is indicated in most patients with acute MI because mild hypoxemia is common. In stable patients, oxygen may be discontinued after 6 hours.
    7. Reperfusion therapy
      1. Thrombolysis These drugs act by promoting the conversion of plasminogen to plasmin, which subsequently lyses thrombi Table 1.5. The principal goal of thrombolysis is prompt restoration of coronary arterial patency.
 
Criteria for Thrombolysis in Acute Myocardial Infarction
 
Indications
  1. Chest pain consistent with AMI.
  2. Electrocardiogenic changes.
    • ST segment elevation > 0.1 mV in at least two contiguous leads.
    • New or presumably new left bundle branch block.
  3. Time from onset of symptoms
    • < 6 hours most beneficial.
    • 6–12 hours lesser but still important benefits.
    • > 12 hours diminishing benefits, but may still be useful in selected patients*.
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Absolute Contraindications
  1. Active internal bleeding (excluding menses).
  2. Suspected aortic dissection.
  3. Recent head trauma or known intracranial neoplasm.
  4. History of CVA known to be haemorrhagic.
  5. Major surgery or trauma < 2 weeks.
 
Relative Contraindications
  1. Blood pressure > 180/110 mm Hg on at least two readings.
  2. History of chronic severe hypertension with or without drug therapy.
  3. Active peptic ulcer.
  4. History of CVA.
  5. Known bleeding diathesis or current use of anticoagulants.
  6. Prolonged or traumatic cardiopulmonary resuscitation.
  7. Diabetic haemorrhagic retinopathy.
  8. Pregnancy.
  9. Prior exposure to streptokinase or APSAC (for initial 6–9 months period after SK or APSAC).
Table 1.5   Characteristics of thrombolytic agents
tPA
SK
APSAC
SCUPA
UK
Fibrin selective
Yes
No
No
Yes
No
Plasminogen activator
Direct
Indirect
Indirect
Direct
Direct
Duration of infusion (min.)
180
60
2–5
90–180
5–15
Early heparin
Yes
No
No
? No
? No
Hypotension
10%
12.5%
Yes
No
No
Allergic reactions
1.6%
5.8%
Yes
No
No
Patency at 90 min.
81–88
53–65
55–65
71
66
Dose (IV)
100 mg over 90 min.
1.5 MU over 60 min. mixed with NS or 5% D
30 U over 2 min.
3 MU over 60 min.
tPA - tissue plasminogen activator; SK - streptokinase; APSAC - aniosylated plasminogen streptokinase activator; scuPA - single chain urokinase plasminogen activator; UK - urokinase.
 
Indications of Successful Thrombolytic Therapy
  1. Resolution of chest pain (23±23 min)
  2. Reduction of ST segment elevation > 50 % within 16±14 min.
  3. Reperfusion arrhythmia—sinus bradycardia, VPCs, accelerated idioventricular rhythm, non-sustained VT. But they are not reliable indicators of coronary revascularization.
  4. Early peaking of cardiac enzymes (due to washout phenomenon in reperfused patients).
  1. Coronary angioplasty
 
Indications
  1. Primary PTCA
    • In patients with contraindications for thrombolytic therapy (specially intracerebral haemorrhage).
    • Patients with cardiogenic shock.
  2. As adjunctive therapy with thrombolysis or in subacute phase of AMI (2–7days) in patients who do not receive thromobolysis.
  3. Rescue PTCA—patients with persistent chest pain and ST segment elevation at 60–90 minutes after the initiation of thrombolytic therapy should be considered for urgent coronary angiography and rescue PTCA.
  1. Emergency CABG—is indicated in patients with refractive ischemia or cardiogenic shock whose coronary anatomy is not suitable for PTCA, in patients in whom PTCA has failed, and in patients with mechanical complications of MI. It is most successful when performed within 6 hrs., which is practically not feasible.
 
Subsequent Management of MI
  1. General Measures
    1. Activity level: Stable patients (free from recurrent chest pain) should have bedside commode privilege immediately and may sit in a chair after 12 hrs. Within first day, patients should be allowed for toileting, assisted bathing and walking in hospital room. After 24–48 hrs., stable patients should progressively increase their activity levels.
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    2. Diet and bowel care
      • No food or drink by mouth until pain free.
      • When pain subsides, allow clear liquids. Subsequently 1200–1800 cal. diet with low cholesterol and no added salts.
      • Routine use of stool softeners and mild laxatives.
    3. Sedation
      • No role of routine administration of anxiolytic drugs.
      • Education and reassurance from hospital staff.
      • Low dose benzodiazepines for narcotic withdrawal.
  2. Additional Pharmacologic Therapy
    Aims:
    i. Reducing thrombolytic and thromboembolic complications.
    ii. Limiting infarct size and recurrent ischemia.
    iii. Favourably affecting ventricular remodelling.
    iv. Reducing short and long-term mortality.
  1. Antiplatelet therapy Aspirin should be given to all patients in the dose of 160–325 mg/day. Patients with contraindications for aspirin like allergy or gastric intolerance, ticlopidine (gpIIb/IIIa receptor inhibitors) 250 mg BD may be given.
  2. Anticoagulation therapy
    1. Heparin should be given IV to all patients who are treated with thrombolytic agents (except streptokinase), are undergoing PTCA or at high risk for developing systemic or venous thromboembolism for at least 48 hours.
    2. IV heparin should be followed by oral warfarin indefinitely in those with AF or severe LV dysfunction and for 3–6 months in patients with an LV mural thrombus or large anterior Q infarct.
    3. Subcutaneous heparin 7500 U BD in patients at low risk for emboli and who are not candidates for reperfusion until the patient becomes ambulatory.
  3. Nitrates to be continued in patients with large Q MI or MI complicated with CHF or recurrent ischemia for 6–12 weeks, dose 10–20 mg BD or 50 mg OD; there should be nitrate free period to reduce nitrate tolerance.
  4. Beta blockers should be continued for long-term unless contraindicated. They reduced the risk of sudden death and reinfarction. Atenolol 50–100 mg/day. Metoprolol 50–400 mg/day. Favourable impact on ventricular remodeling improvement of ejection fraction and reduction in CHF and reduction in ischemic event and reinfarction.
  5. ACE Inhibitors
    1. When initiated within the first 24 hours, they provide a reduction in short-term mortality by improving EF and preventing LV dilatation. The benefits of beta blockers are greatest in the first year post-infarct, while the sensitivity of ACE are most evident by the second or third years.
    2. After 4–6 weeks, ACE inhibitors can be discontinued in patients with normal or mildly decreased LV function. Patients with CHF or asymptomatic LV dysfunction (EF < 40per cent) should receive ACE inhibitors indefinitely.
  6. Calcium channel blockers No mortality benefit, may be associated with excess mortality or increased incidence of reinfarctions (specially with nifedipine).
 
Risk Stratification and Revascularization
Risk factors are : 1) History of previous MI; 2) Sustained hypotension or cardiogenic shock; 3) Early ventricular arrhythmias with hemodynamic compromise; 4) CHF; 5) Advanced heart block; 6) Recurrent post MI angina; 7) EF<40%.
  1. High risk patients : Having one or more risk factors. These patients should remain hospitalized for several days after their condition has stabilized and should undergo coronary angioplasty.
  2. Low risk patients: patients who do not fit into the high risk group, can be discharged after 3–4 days and are subjected to submaximal stress test on day 4 or maximal stress 10test at 2–3 weeks. Patients with inducible ischemia should be considered for surgical or percutaneous revascularization.
 
COMPLICATIONS OF MI (Tables 1.6 to 1.9)
  1. Ventricular Dysfunction Following MI, the left ventricle begins to dilate both in infarcted and non-infarcted regions. This is called ventricular remodeling and generally precedes the development of CHF. This remodeling may be ameliorated by therapy with ACE inhibitors and other vasodilators (e.g. nitrates).
  2. Cardiogenic Shock Is defined as a systolic BP < 80 mmHg in the presence of organ hypoperfusion. Typically, patients who develop cardiogenic shock have severe multi-vessel coronary artery disease with ‘piecemeal necrosis’ extending outwards from the infarct zone. Infarction of ≥ 40% of left ventricle usually results in cardiogenic shock.
 
 
Cause
  1. In 80% cases, cause is extensive damage to the left ventricular myocardium.
  2. Remaining 20% -mechanical defect like ventricular septal or papillary muscle rupture or predominant right ventricular myocardial infarction.
Presentation 10% of patients with cardiogenic shock present at the time of admission, where as 90% develop during hospitalization (due to infarct extension).
Risk factors Old age, history of prior MI or CHF, anterior wall infarction.
Diagnosis Cardiogenic shock is characterized by:
  1. Marked and persistent (> 30 min) hypotension and systolic BP < 80 mmHg.
  2. Cardiac index < 1.8 litres/min/m2.
  3. Elevated left ventricular filling pressure (PCWP) > 18 mmHg. Prognosis is poor with mortality ≥ 70 %.
Table 1.6   Doses of dopamine, dobutamine and amrinone
Dose
Mechanism of Action
Dopamine
Start with 2–5 |ig/kg/min; increase every 2–5 hr. upto a maximum of 20–30 jig/kg/min
2–10 jig/kg/min. →positive chronotropic and ionotropic effects (due to P receptors stimulation). > 10 jig/kg/min. →vasoconstrictor effects (a receptor stimulation).
Dobutamine
2–10 jig/kg/min. Occasionally upto 40 jig/kg/min for max of 72 hrs. contraindicated BP < 70 mmHg
Positive ionotropic and minimal positive chronotropic or peripheral constrictive activity in dose of 2.5–10 Hg/kg.
Amrinone and Milrin-one
Amrinone-loading dose 0.75 mg/kg followed by 5–10 |ig/kg/min. Milrinone.
Positive ionotropic agents without catecholamines structure or activity that act by inhibiting phosphodiesterase.
 
Management
The primary objective of treatment is to maintain coronary perfusion by raising the arterial BP with vasopressors, intra-aortic balloon counterpulsation and manipulation of blood volume to a level that ensures an optimum left ventricular filling pressures. In patients seen within the first 4–8 hours, PTCA is a better choice Table 1.6.
  1. Vasopressors
  2. Intra-aortic Balloon Counterpulsation May be useful in patients with cardiogenic shock due to mechanical defects following AMI or to severe left ventricular dysfunction when other mechanical measures fail.
  3. Reperfusion Reversal of cardiogenic shock by acute reperfusion has been reported, usually with thrombolytic therapy, emergency PTCA, or a combination of these measures.
  1. Right Ventricular Myocardial Infarction (RVMI) Approximately 1/3rd of patients with inferoposterior MI demonstrate at least a minor degree of right ventricular MI. It is associated with anterior wall MI in approximately 8 % of cases. Isolated right ventricular MI is very rare (about 1per cent of all cases of right ventricular MI).
    11
 
Diagnosis
  1. Clinical presentation The clinical triad of hypotension, hunged hepatojugular reflux and clear lung fields in the setting of inferior MI are highly suggestive of RVMI.
    Other features Bradycardia or heart block, Kussmaul's sign, pericardial friction rub, TR, right sides S3 or S4.
  2. ECG ECG changes usually persist for 18–36 hours. These are following :
    1. ST elevation ≥ 1.0 mm in V4R-100% sensitive and 68 % specific.
    2. ST elevation in lead V1 with ST depression in V2.
    3. ST depression in lead V2 ≤ 50% of ST elevation in aVF.
    4. ST elevation in lead III > lead II.
    5. ST elevation in lead V1 to V3.
  3. Echocardiography Consistent with right ventricular (chamber dilatation, regional wall motion abnormalities, or impaired systolic function).
  4. Hemodynamic findings Gold standard— for the clinical diagnosis of right ventricular MI. Findings include-low cardiac output, elevated right atrial press, elevated right ventricular end-diastole pressure, normal or slightly increased PCWP.
Table 1.7   Mechanical complications of MI
Variables
VSD
Free Wall Rupture
Papillary Muscle Rupture (MR)
Days post MI
3–5
3–6
3–5
Anterior MI
60%
50%
25%
Systolic murmur
90%
25%
30%
Palpable thrill
Yes
No
Rare
Previous MI
25%
25%
30%
Mortality
Medical
90%
90%
90%
Surgical
30%
40–90%
 
Differential Diagnosis
  1. Hypotension with AMI
  2. Pericardial tamponade.
  3. Constrictive pericarditis
  4. Pulmonary embolism
 
Treatment
  1. Reperfusion therapy in appropriate patient.
  2. Expanding plasma volume by normal saline 1 to 3 litres in the first hours after MI and then 200 ml/hr to augment right ventricular preload and C.O.
    Table 1.8   Cardiac arrhythmias and their management during AMI
    Category
    Arrhythmia
    Therapeutic Option
    Electrical instability
    Ventricular premature beats
    Potassium and magnesium solution, beta blockers.
    Ventricular tachycardia
    Antiarrhythmic agents, cardioversion / defibrillation.
    Ventricular fibrillation
    Defibrillation, bretylium tosylate
    Accelerated idioventricular rhythm
    Increase sinus rate (atropine, atrial pacing), antiarrhythmic agents.
    Non-paroxysmal AV junctional tachycardia
    Atrial overdrive pacing; antiarrhythmic agents; cardioversion
    Pump failure / excessive sympathetic stimulation
    Sinus tachycardia
    Antipyretics, analgesics, beta blocker, treat CHF if present
    Atrial fibrillation and/or flutter
    Verapamil, digitalis, glycosides, anti CHF measures, pacing for flutter
    PSVT
    Vagal maneuvers, verapamil, cardiac glycosides, beta blockers, cardioversion
    Bradyarrhythmias and
    Sinus bradycardia
    Atropine, atrial pacing
    conductive disturbances
    Junctional escape rhythm
    Atropine, atrial pacing
    AV block and interventricular block
    Insertion of pacemaker
    12
    Table 1.9   Other complications of AMI
    Complications
    Cause
    Therapy
    Recurrent chest pain (25% of AMI)
    Extension of the original infarct or reinfarction in new zone.
    Repeat therapy or coronary revascularization.
    Pericarditis*
    Association with transmural MI
    Aspirin 650 mg qid
    Anticoagulants are contraindicated.
    Thromboembolism (10% of AMI)
    Association with large anterior infarcts, CHF, LV thrombus
    Systemic anticoagulation upto 3–6 months
    LV Aneurysm (<5–10% of AMI)
    Association with large anterior transmural AMI (with total occlusion of poorly collate related LAD artery). Persistent ST segment elevation in ECG > 3 months suggest aneurysm formation.
    Aggressive management of AMI prevent aneurysm formation. Aneurysmectomy.
    * Post myocardial infarction syndrome or Dressler's syndrome - characterized by fever and pleuropericardial chest pain, is thought to be due to an autoimmune pericarditis, pleuritis and/or pneumonitis. It may begin from a few days to six weeks after MI and usually responds promptly to therapy with salicylates.
  3. Vasodilators-e.g. Dobutamine, Nitroprusside, when cardiac index not improved after saline infusion (when LV failure is present).
  4. PTCA/intra-aortic balloon counterpulsation-when low output state not improved after volume expansion or with vasodilators.
  5. Avoid preload reducing agents such a diuretics, nitrates, morphine.