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In approximately 30% of patients with Q-wave inferior wall MI, there is associated right ventricular infarction. Rarely, it can occur with anterior wall MI.

Clinical Features Hypotension Pulsus paradoxus Raised JVP Kussmaul’s sign Clear lungs RV S3 and S4 Fig. 3.142: LV aneurysm

TR murmur

Enlarged, tender liver. Treatment

• Diuretics are contraindicated.

• IV fluids are given to counteract the hypotension.

Management

1. Bed-rest 2. Nasal O2

3. Morphine given in an intravenous form (< 1 mg per minute) to a maximum dose of 10–15 mg. It acts as a pulmonary venodilator and also as an analgesic to alleviate anxiety

4. Nitrates may be given sublingually for rapid action of relief of pain by coronary vasodilation. It also helps to reduce the preload of the heart, being a predominant venodilator. If pain persists after administration of sublingual nitrates, IV infusion of nitroglycerine may be given, provided the sys- tolic BP is maintained above 100 mm Hg

5. Aspirin is given orally in the dose ranging from 100 to 300 mg

6. Thrombolytic therapy (Streptokinase, Urokinase, Tissue plasminogen activator) may be given and is particularly useful if given within 6 hrs of onset of

Comparison of Anterior and Inferior Wall Myocardial Infarction

Features Anterior MI Inferior MI

1. Extent of necrosis Large Small

2. Extent of coronary atherosclerosis Small Large

3. Complications

a. Ventricular septal rupture Apical, easily repaired Basal, difficult to repair

b. Aneurysm Common Uncommon

c. Free wall rupture Uncommon Rare

d. Mural thrombus Common Uncommon

e. Heart blocks Uncommon Common

f. Bundle branch blocks Common Uncommon

4. Prognosis Worse than that of inferior MI Better than that of anterior MI

5. Diagnosis

a. Symptoms Gastrointestinal symptoms unusual Gastrointestinal symptoms (nausea,

vomiting, hiccough) common b. Physical examination Tachycardia; hypotension uncommon. Bradycardia; hypotension common.

Jugular venous distention less Jugular venous distention common. common than with inferior MI. 20% have S3

50% have S3

c. ECG Features of anterior wall MI Features of inferior wall MI

d. Echocardiogram Abnormal left ventricular wall Abnormal left ventricular wall motion motion is anterior in location. is inferior in location. Right ventricular No abnormal right ventricular abnormal wall motion present in

wall motion approximately one-third of patients.

symptoms, but may be given upto 12 hrs after onset of symptoms.

Ideal—door to needle time 30 min.

Thrombolytic agents for Myocardial Infarction

Agents with fibrin specificity:

1. Alteplase (rt-PA) 15 mg IV bolus followed by 0.75 mg/kg IV infusion (upto 50 mg) over 30 minutes then 0.5 mg/kg (upto 35 mg) by IV infusion over 60 minutes (maximum dose 100 mg IV over 90 minutes)

2. Reteplase (r-PA) 10 mg IV bolus over 2 minutes followed by another 10 mg IV bolus after 30 minutes.

3. Tenecteplase (TNK-tPA) 0.5 mg/kg IV bolus (<60 kg-30 mg, 61-70 kg -35 mg, 71-80 kg-40 mg, 81-90 kg- 45 mg, >90 kg-50 mg)

Agents without fibrin specificity:

1. Streptokinase – 1.5 million units IV infusion over 60 minutes

2. Urokinase

Because of the development of antibodies, patients who were previously treated with strepto- kinase should be given an alternate thrombolytic agent.

Contraindications for Thrombolytic Therapy

Absolute contraindications:

Active bleeding Defective haemostasis

Recent major trauma

Surgical procedures < 10 days Invasive procedures < 10 days Neurosurgical procedure < 2 months GI/genito-urinary bleeding < 6 months Stroke/TIA < 12 months

Prolonged CPR > 10 minutes

H/O CNS tumour, aneurysm, AV malformation Active peptic ulcer

Aortic dissection Acute pericarditis

Active inflammatory bowel disease Active cavitary lung disease Pregnancy

Relative contraindications:

Systolic BP > 180 mm Hg Diastolic BP >110 mm Hg Bacterial endocarditis

Haemorrhagic diabetic retinopathy

H/O intraocular bleeding Chronic warfarin therapy Severe renal or liver disease Severe menstrual bleeding

Beta blockers can be used in LV dysfunction with low ejection fraction whereas calcium channel blockers should not be used. ACE inhibitor is the ideal choice in the presence of LV dysfunction and cardiac failure with normal renal function. 7. Heparin may be given in a dose of 5000 U, 12

hourly, subcutaneously, as prophylaxis against development of deep vein thrombosis and 12,500 U, 12 hourly, subcutaneously, as prophylaxis against development of mural thrombus or exten- sion of the coronary thrombus, for a period of 7–10 days

8. β-blockers are started immediately, or after two weeks and given for a minimum duration of two years, if there is no contraindication for their use, Commonly used Drugs in CAD–ACS/MI

Drugs Clinical condition Contraindication Dosage

Nitrates Angina/equivalents Hypotension Infusion – 5-10 μg/min

Titrate upto 75-100 μg/ min or Topical/oral/buccal

Beta blockers Unstable angina ACS/MI/ Heart rate < 60/min AV – Metoprolol 5 mg IV

Secondary prevention, block, ShockBP < 90 mm Hg Repeat every 5 min

Angina inspite of nitrates COPD, CCF upto 15 mg and then

oral 25-50 mg/bid

Esmolol 0.1 mg/kg/min/IV

Morphine sulphate Persistent pain Hypotension, Respiratory 2-5 mg IV

depression/confusion Repeat 5-30 min as needed

ACE inhibitors LV-dysfunction Hypotension Captopril/Enalapril

EF < 40%, H. failure Renal insufficiency Ramipril (avoid IV)

Warfarin Atrial fibrillation

LV-dysfunction Bleeding manifestations 5-10 mg to maintain INR

thrombus/emboli of 2-3

Calcium channel blockers Variant angina Pulmonary oedema Avoid short acting

Recurrent ischaemia LV dysfunction nifedipine

Anti-ischaemic Drugs—Mechanisms of Action

Action Nitrates β-blockers Ca-blockers

Decreased myocardial demand ++ +++ + to ++

Increased coronary blood supply +++ 0 to + ++ to +++

Prevent coronary spasm or vasoconstriction ++ 0 ++ to +++

Left ventricular function Improves 0 0

Other actions Antiplatelet action and Electrical stabilisation Antihypertensive

Normalises endothelial and antiarrhythmic

Salmonella Tuberculosis

β haemolytic streptococci Meningococci

Leptospirosis

Viral Coxsackie B virus

HIV Influenza Poliomyelitis

Viral hepatitis C and adeno virus Cytomegalo virus Epstein-Barr virus Fungal Candida Cryptococci Blastomyces Aspergillus Rickettsia R. typhi (typhus)

R. tsutsugamushi (scrub typhus)

Chlamydia C. psittaci

Protozoal Trypanosomiasis

Toxoplasmosis

HypersensitivityAcute rheumatic fever states

Physical agents Radiation, heat stroke Chemicals Cobalt, antimony, arsenic Drugs Phenothiazines, tricyclic

antidepressants, emetine, penicillin, methyldopa

Unknown Fiedler’s giant cell myocarditis. Myocarditis may progress to dilated cardiomyopathy.

Clinical Features

Fatigue, angina, dyspnoea, inappropriate or dispro- portionate tachycardia, heart failure.

On Examination

Muffled S1, S3, MR murmur, pericardial friction rub. ECG

Disproportionate tachycardia; transient ST-T changes; various conduction defects can occur including atrial or ventricular ectopics.

Contrast MRI

It reveals contrast enhancement.