Patient: Sukh Ram | Serial No. 9215126002272493

Diagnosis (Decoded)

Primary Diagnosis

• CAD = Coronary Artery Disease
• ACS = Acute Coronary Syndrome
• STEMI = ST-Elevation Myocardial Infarction (a "full blockage" heart attack)
• IW = Inferior Wall (the bottom portion of the heart, supplied by the RCA)
• RV = Right Ventricular involvement (the right ventricle is also infarcted)

Secondary Finding

• Killip Class I = No signs of heart failure (no rales, no S3 gallop) - relatively preserved cardiac function on presentation
• TIMI 7/14 = A moderate-to-high risk score on the TIMI risk stratification for STEMI, indicating significant risk of adverse outcomes

Clinical Course (Decoded)

Finding 1: NSR → Paroxysmal AF → Sinus Pause + P/CPR

• Patient initially had Normal Sinus Rhythm (NSR)
• Developed Paroxysmal Atrial Fibrillation (AF), a known complication of RV infarction
• This led to a Sinus Pause (prolonged absence of heartbeat), requiring CPR

Finding 2: Sustained Monomorphic VT + P/DC shock

• Patient developed Sustained Monomorphic Ventricular Tachycardia (VT) - a life-threatening arrhythmia
• Treated with DC (Direct Current) cardioversion/defibrillation shock - emergency electrical treatment to restore normal rhythm

Finding 3: RWMA @ RCA Territory

• Regional Wall Motion Abnormality (RWMA) detected in the RCA territory
• RV dysfunction confirmed (Right Ventricle not pumping adequately)
• Low LVEF (Left Ventricular Ejection Fraction also reduced)

Procedures Performed

CAG-TVD (Coronary Angiography - Triple Vessel Disease)

• LAD (Left Anterior Descending) - TCO (Total Chronic Occlusion)
• LCx (Left Circumflex) - P 7/17, Gm mg 90% stenosis (~90% blockage)
• RCA - p TCO (proximal Total Chronic Occlusion) - this is the culprit vessel

P/PTCA to RCA

• PTCA (Percutaneous Transluminal Coronary Angioplasty) was performed on the RCA - a balloon was used to open the blocked artery, restoring blood flow

Medications Prescribed (Rx)

Summary

1. Paroxysmal AF with sinus pause requiring CPR
2. Sustained monomorphic VT requiring DC cardioversion

Note: RV infarction in the context of inferior STEMI - as noted by the ACC (2024) - occurs in ~50% of inferior STEMIs, with the culprit nearly always being proximal RCA occlusion causing RV free wall dysfunction.

Hospital Continuation Sheet — Date: 15/6/26

Diagnosis (Decoded)

Primary Diagnosis

• CAD = Coronary Artery Disease
• Recent STEMI = ST-Elevation Myocardial Infarction that occurred recently (not acute/ongoing, but within the recent past - typically within days to weeks)

Risk Stratification

Killip II, TIMI 4/24

• Killip Class II = Mild heart failure present - there are signs such as S3 gallop, basal rales (crackles in lungs), or elevated JVP, but no pulmonary edema yet. This is a step up from the previous patient's Killip I, indicating some degree of LV dysfunction.
• TIMI 4/24 = A moderate risk score on the TIMI STEMI risk scale

Clinical Complications (Decoded)

1. Junctional Bradycardia → AF → JSVT

• Junctional Bradycardia - The SA node failed, so the AV junction took over as pacemaker, producing a slow heart rate. This is a recognized complication of inferior STEMI (vagal tone increase + ischemia of the AV node, which is supplied by the RCA in ~90% of people).
• → AF - Progressed to Atrial Fibrillation (chaotic atrial rhythm)
• → JSVT - Then to Junctional Supraventricular Tachycardia (a rapid rhythm originating at or near the AV node)
• On/Off TPR = Transient episodes, possibly with TPR referring to Temporary Pacing Rate or Total Peripheral Resistance changes noted

2. Global Hypokinesia

• On echocardiography: all walls of the heart are moving poorly (not just one territory)
• This indicates diffuse LV dysfunction, suggesting either extensive infarction, multi-vessel ischemia, or stress cardiomyopathy superimposed on the STEMI
• Associated with mild LVH (Left Ventricular Hypertrophy) and mild MR/TR (Mitral Regurgitation / Tricuspid Regurgitation) - functional valve leaks due to poor ventricular geometry

3. 2° CNA (Confirmed)

• Likely Secondary Central Nervous System/Neurological involvement - possibly CNA = Cerebrovascular/Neurological event or CNA = Cardiogenic Non-oliguric AKI related note - this is partially illegible but "confirmed"

4. i AKI (Acute Kidney Injury)

• AKI = Acute Kidney Injury - a serious and common complication after STEMI
• Caused by reduced cardiac output (low perfusion to kidneys), contrast nephropathy from angiography, or diuretic use
• The "i" likely means ischemic AKI - the kidneys are underperfused due to cardiogenic low-output state

Vitals

Treatment Plan

Type C (likely referring to a care pathway or protocol level)

• CVS S1-S2: Normal heart sounds heard (first and second sounds present)
• S2 = (3rd sound?): Possible S3 gallop - supports Killip II classification
• B/L Rhonchi = Bilateral rhonchi (wheezing/rattling sounds) in both lungs - indicating pulmonary congestion or bronchospasm from fluid overload, consistent with Killip II

Summary

Patient: Swaksha / Suraksha (F) | CR No. 9315126009378378

CHIEF COMPLAINTS

• Syncope - 3 episodes, yesterday (13/6/26)
• Patient was apparently well till morning of 13/6/26
• Had 3 episodes of LOC (Loss of Consciousness) lasting a few seconds
• After each episode: self-fall and regaining of feet/consciousness
• No convulsions (noted separately)

CO-MORBIDITIES (Right side of page 1)

PAST HISTORY

• No history of cardiac palpitations (no prior cardiac symptoms)
• No prior seizure/convulsion episodes
• No blurring of vision / dizziness
• Not worse on postural change (rules out pure orthostatic hypotension as sole cause)
• No tinnitus / vertigo
• No chest pain

FAMILY HISTORY

• Has SOR (possibly shortness of breath), NYHA class - for IP (inpatient)

PERSONAL/SOCIAL HISTORY

• Moves in winter/summer (seasonal activity)
• H/O fever (101°F) < 2 days, no cough, no burning micturition

PAGE 2 - EXAMINATION FINDINGS

General Physical Examination

• Conscious, alert
• P/+/Cy/Cl/Oe = Pallor absent / Icterus absent / Cyanosis absent / Clubbing absent / Oedema absent

Vitals

SYSTEM EXAMINATIONS

CVS (Cardiovascular System)

• CNS: Apex NP (Apex not palpable or normal position)
• No palpable thrill
• S1-S2 normal

ECG Findings (circled - key finding):

• NSR (Normal Sinus Rhythm)
• HR: 72/min (ECG rate - different from peripheral PR of 28, suggesting pulse deficit / complete heart block)
• PR interval: >200 ms - First or Higher degree AV Block
• QRS: broad - conduction abnormality
• Q waves - suggesting old/recent infarction

Respiratory System

• ET: soft
• B/L air entry: bilaterally reduced
• A/Z Hz (likely Adventitious sounds)
• No S3/murmur

ECHO Findings (circled):

• All valves and chambers normal (W)
• Trivial MR/TR (Mitral/Tricuspid regurgitation - trivial, not significant)
• WCY RWS A (Wall motion normal)
• MAC (+) = Mitral Annular Calcification - associated with elderly/diabetics

Nervous System

• B/L 4 limbs: No weakness

Musculo-skeletal System

• Kyphosis ILS (kyphosis present)

Endocrine System

• Clinically Euthyroid (despite hypothyroidism history, clinically compensated)

PROVISIONAL DIAGNOSIS

Syncope secondary to Complete/High-degree AV Block

• Heart rate of 28/min (pulse rate) with an ECG showing PR >200ms and broad QRS = likely Complete Heart Block (CHB) or High-degree AV Block
• The AV node is failing to conduct impulses from atria to ventricles properly; the ventricles are running on a slow escape rhythm at 28 bpm, causing recurrent syncope (Stokes-Adams attacks)
• This is compounded by BP 100/60 (hemodynamic compromise from the bradycardia)

Differential Diagnoses:

1. Complete Heart Block (CHB) / Stokes-Adams Syncope - most likely (PR >200ms, HR 28, broad QRS, syncope)
2. Vasovagal syncope - less likely (no precipitating trigger noted, HR 28 is too slow)
3. Sick Sinus Syndrome - possible given age + DM + comorbidities
4. Hypoglycemic episodes - less likely but RBS is 440 (hyperglycemic, not hypoglycemic)
5. Seizure disorder - excluded (no convulsions, no post-ictal confusion)

Contributing Factors:

• DM × 20 years - autonomic neuropathy can affect cardiac conduction
• HTN × 20 years - hypertensive heart disease + MAC on echo
• COAD - hypoxia contributing
• Hyperglycemia (RBS 440) - metabolic derangement worsening conduction

Summary

Patient: Gurkan / Gurkan Sain | 64 yr / Male | CR No. 9215126009278416

PAGE 1 - HISTORY

Chief Complaint

• Chest pain at ~6:30 PM on 19/6/26
• Sudden onset while the patient was sleeping
• Pain character: Retrosternal, diffuse
• Intensity: Moderate to severe
• Radiation: To both arms (bilateral)
• Associated symptoms: Sweating (+), Nausea/Vomiting (+), SOB (+), Palpitations (+), Dizziness (+)

Co-morbidities (right column)

Past History

• Went to Rampur / Rekhanei hospital previously
• Thrombolysed (given clot-busting drug - fibrinolytic therapy) × TWK at 9 AM (i.e., thrombolysis was done within the time window)
• ECG at time: ST↑ V4-V6 (ST elevation in leads V4-V6 = Anterior/Lateral STEMI)
• Now referred to AIIMS Chandigarh (tertiary care referral)

Social/Personal History

• At the time of chest pain onset: ~40? (age or onset note)
• No SOB / palpitations
• No history of fever / cough / active bleeding

PAGE 2 - EXAMINATION & INVESTIGATIONS

General Physical Examination

• Conscious, anxious
• P/+/Cy/Cl/Oe = No pallor/icterus/cyanosis/clubbing/oedema

Vitals

CVS Examination

• Apex 5th ICS @ midclavicular line - normal position
• Non-sustained (likely a brief arrhythmia noted)
• No thrill, no murmur

Key Investigation Results (right side, page 2)

ECG Findings

• NSR (Normal Sinus Rhythm)
• HR: 76/min
• QS in V1-V5 - deep Q waves indicating completed anterior infarction
• ST↑ in V4-V6, I, aVL - ongoing anterior/lateral STEMI pattern
• Q waves in III, II, aVR (inferior territory involvement possible)
• T waves: aVL - changes present

ECHO Findings (Echo report - left side page 2)

• Conc. LVH = Concentric Left Ventricular Hypertrophy
• RWMA (Regional Wall Motion Abnormality) = Anterior wall not moving - LAD territory
• Apical-akinetic = Apex is not contracting (akinesis) - LAD occlusion hallmark
• Mild LVD (Left Ventricular Dysfunction)
• Normal RVs R (Right ventricular size and function normal)
• Trivial MR (Mitral Regurgitation - trivial)
• IVC = 18mm, PSON RV (IVC dilated - elevated RA pressure)

DIAGNOSIS

Primary Diagnosis:

• Culprit vessel: LAD (Left Anterior Descending artery)
• ST elevation in V1-V6, I, aVL with QS pattern = classic anterior STEMI
• Already thrombolysed at peripheral hospital (9 AM)
• Troponin I = 279 - confirms extensive myocardial damage
• ECHO: Apical akinesis + anterior RWMA + mild LVD - structural damage consistent with LAD occlusion

Secondary Diagnoses:

TREATMENT PLAN

Immediate / Acute Management

1. Dual Antiplatelet Therapy (DAPT): Aspirin + Clopidogrel/Ticagrelor - continue from thrombolysis protocol
2. Anticoagulation: LMWH (Enoxaparin) or Unfractionated Heparin - per post-thrombolysis protocol
3. Statin: High-intensity - Rosuvastatin 40mg or Atorvastatin 80mg OD
4. Beta-blocker: Metoprolol/Carvedilol - for LV protection (once hemodynamically stable)
5. ACE Inhibitor/ARB: Ramipril - for LV remodeling prevention (caution: CKD present)
6. Oxygen: Maintain SpO2 >95%

Urgent Cardiology Workup

1. CAG (Coronary Angiography): Urgent/early (within 24 hours of thrombolysis if not reperfused, called "pharmaco-invasive strategy") - to assess LAD patency and decide on rescue PTCA/PCI if thrombolysis failed
2. Echocardiogram follow-up: To reassess LV function post-reperfusion
3. Serial ECGs and Troponins - to assess reperfusion success

Ongoing Management

1. Tight glycemic control (DM present) - insulin sliding scale
2. Renal monitoring - CKD baseline, contrast precautions before CAG (hydration, N-acetylcysteine)
3. Smoking cessation counseling
4. Lipid management - target LDL <70 mg/dL post-MI
5. Cardiac rehabilitation after discharge

Summary