A 58 yr old male known hypertensive since 10 yrs and diabetic since 3 yrs on regular medication comes to emergency dept with sudden onset of grade 4 dyspnea, with profuse sweating, no chest pain from 2hrs, on arrival to ED patient is tachypneic RR 34,tachycardic 124,BP 110/70mm of hg, SPo2 85 %in RA, GRBS 279 mg/dl, On systemic exam, CNS Pt is conscious oriented CVS s1 s 2 present, RS b/l air entry present b/l crepts, P/A soft, please diagnose and management

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The patient presented with acute pulmonary edema This ECG demonstrates the classical pattern of left main coronary artery (LMCA) occlusion: Widespread horizontal ST depression, most prominent in leads I, II, avl, avf, and V2-6 ST elevation in aVR 1mm ST elevation in aVR V1 However, ST elevation in aVR is not entirely specific to LMCA occlusion. It may also be seen with: Proximal left anterior descending artery (LAD) occlusion Severe triple-vessel disease (3VD) Diffuse subendocardial ischaemia e.g. due to O2 supply/demand mismatch, following resuscitation from cardiac arrest Some authors argue that using the term LMCA occlusion is inaccurate, as most of these patients have at least some flow in their LMCA (i.e. incomplete LMCA occlusion); whereas a complete LMCA occlusion would rapidly lead to STEMI, cardiogenic shock and death. Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6; therefore ST depression in these leads will produce reciprocal ST elevation in aVR. Lead aVR also directly records electrical activity from the right upper portion of the heart, including the right ventricular outflow tract and the basal portion of the interventricular septum. Infarction in this area could theoretically produce ST elevation in aVR. ST elevation is aVR is therefore postulated to result from two possible mechanisms: Diffuse subendocardial ischaemia, with ST depression in the lateral leads producing reciprocal change n aVR (= most likely). Infarction of the basal septum, i.e. a STEMI involving aVR. The basal septum is supplied by the first septal perforator artery (a very proximal branch of the LAD), so ischaemia / infarction of the basal septum would imply involvement of the proximal LAD or LMCA. In the context of widespread ST depression + symptoms of myocardial ischaemia: STE in aVR 1mm indicates proximal LAD / LMCA occlusion or severe 3VD STE in aVR 1mm predicts the need for CABG STE in aVR V1 differentiates LMCA from proximal LAD occlusion Absence of ST elevation in aVR almost entirely excludes a significant LMCA lesion In the context of anterior STEMI: STE in aVR 1mm is highly specific for LAD occlusion proximal to the first septal branch In patients undergoing exercise stress testing: STE of 1mm in aVR during exercise stress testing predicts LMCA or ostial LAD stenosis Magnitude of ST elevation in aVR is correlated with mortality in patients with acute coronary syndromes: STE in aVR 0.5mm was associated with a 4-fold increase in mortality STE in aVR 1mm was associated with a 6- to 7-fold increase in mortality STE in aVR 1.5mm has been associated with mortalities ranging from 20-75%

Very informative thanks
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Dear Dr.Shivaji, when ever Ur mentioning Grading for dyspnea...U should always Name the Grading like for Respiratory it's MMRC Grading or If underlying Cardiac disease it's NYHA Grading...bcoz all these Grading are not alike. In CVS examination, U should comment on S1 and S2 character rather than Present...bcoz they are always present in all patients. ABG s/o Mixed Acid Base disorder Metabolic Acidosis associated with Respiratory Acidosis It's an High Anion Gap Metabolic Acidosis and DELTA GAP is Zero So, rule out Diabetic KetoAcidosis in this patient. (ketones in urine) Ecg s/o Sinus tachycardia, Normal Axis, PR /Qrs normal, No Chamber hypertrophy, ?St elevation in AVR > V1 with St depression in remaining all chest and precordial leads...So, Could be a Left Main Disease... So send Troponins, if positive then Treat As STEMI and refer to PCI (If Feasible) by loading pt with Dual Antiplatelet s, High Intensity statins and Heparin... If PCI not possible , then thrombolyse... Left Main disease mostly doesn't respond to fibrinolytic s most of the time. Simultaneously, check for S.potassium , S.Magnesium, Ca. In cases of dyselectrolytemia, correct them accordingly...as even hypokalemia may produce such ecg changes or can be concomitant. CXR PA view, Cardiomegaly, with left cardio phrenic angle minimal blunting with cephalisation of vessels in upper zones representing Pulmonary venous Hypertension with Interstitial edema... So,look for signs of Acute LVF following MI involving Left Main disease with ?DKA

Thank you for your suggestions Dr Sandeep, but for an emergency physician, in a busy and chaotic ED, securing the Airway breathing and circulation are the priorities and approaching to differential diagnosis is more important than listening to the character of heart sounds and grading of dyspnea, which is not possible in busy ED and it will not alter the management of patient in ED, more it might be imp for a cardiologist in opd to approach to a diagnosis
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patient seems to have pulmonary odema which seems be due to cardiac dysfuntion as there is st depression in v 2 to v6 . patient can also have renal impairment also as long standing diabetes.so management includes send cbc rft lft cardiac enzymes .case to be seen by interventuonal cardiologist .mean while intubate and ventilate the patient on pressure control ventilation and give acs cocktail get blood ketones and urine ketones done .manage rbs on sliding scale .resend arterial blood gas analysisand if acidosis give bicarbonate. give loop diuretics and maitain bp on noradrenaline infusion .if coronary angiography reveals any blockage get angioplasty done . if established renal failure with anuria get haemodialysis done

We should not give bicarbonate incases of pulmonary edema.... bicarbonate is hygroscopic and leads to further precipitation of LVF
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X-ray show Pulmonary Odema ecg show Widespread st depression with St elevation in avr, v1 D / D Demand supply mismatch lf main or three vessel dieases stat echo followed by Rx of pulmonary Odema & do serial ecg to see weather these changes persist or go away

Anteriolateral wall infarction with miliary pulmonary koch's, advised ICU management.

acute LVF with pulmonary oedema treat with diuretics ntg LMWH dual antiplatelet bipap ventilation proximal LAD lesion tight glycaemic control

st elevation in avr LMCA stenosis
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Nice case discussion . Thanks

Welcome Dr neeraj
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Dx acute pulmonary edema rx O2 inhalation. inj lasix.

ami with acute pulmonary edema. O2 inhalation. inj lasix. inj opioid

nstemi ,anterolateral , preceding to pulmonary edema ,and is mixed acidosis ,sugar will be slightly raised so not to worry ,your pt might soon go in cariogenic shock so give all loading dose and start ntg low dose then ,nikoran infusion ,,lasix infusion ,dobutamine infusion and if pt is conscious put him on bipap also start lmwh

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