Orris

I'm attached to the cardiology ward. I need to present this case in great detail, as my preceptor is very strict, and I need to have a very good understanding of the case and all guideline-based recommendations, such as CPG Malaysia, and so on.Ill need a very good understanding of the disease, medication, why what all the 7W questions.Pls discuss all general available treatment as well for this case so i know what other choices of medicines are also available and the suitability Usually, the flow of the presentation goes like: Flow of presentation: 1. Patient, age, gender 2. ⁠what is the chief complaint 3. ⁠what is the diagnosis 4. ⁠on day 1 admitted, wht problem then give what medication, indication for what, then is it appropriate to give the med for this problem, any more better option? (No pci then skip nxt day- same flow summary - until the last day) 5. ⁠next day, some symptoms resolve, dr stop certain medication due to …. Then some other problem arise and dr prescribe ….. the indication for the medication is for …… is it appropriate….. 6. ⁠overall no PCI in this case / u found some pci and need some clarification….. 7. ⁠thank you but rather than solely mentioning if the medications are appropriate or not, it would be better to state the indications. For eg, this pt was started on Tab pantoprazole 40mg BD for (indication) from (duration). Then if anything was found inappropriate/incorrect, it can be mentioned as a PCI & then explain accordingly. Your flow is correct. Just follow the CP2 sections. Ill attach the CP2 form. But some preceptor wants it to b like a story telling like : 1. Patient, age, gender 2. ⁠what is the chief complaint 3. ⁠tell the diagnosis , then the medicines instead of the medicine first then the indication. And carry on with the flow So i want u to generate 2 types of complete script for my presentation Patient name: NS Age: 64 years Sex: Female Underlying: DM HPT CKD stage 3A HFrEF for investigation to rule of ischemic cause ECHO done on 4/2/26: LVEF 32%, RWMA global hypokinesia Plan for NPS viability study KIV COROS (Pls explain more about this) +- PCI Last admission in April 2026 for Decomp HFrEF TRO abdominal malignancy -Ca 125: 257 (whats this) - other tumour marker not raised -S/B gynae: limited TAS finding to get USG abdomen USG abdomen 27/4/26: Impression: Fatty liver with hepatomegaly B/L renal parenchymal disease Right pleural effusion with mild ascites No abdominal mass / collection Patient old meds: T.Lasix 40 mg OD T. Bisoprolol 2.5 mg OD T. Atorvastatin 40 mg OD T. glyprin 1/1 OD S/C mixtard 18/20 unit T. pantoprazole 40 mg OD Panel Parameter (Normal Range) 15/4/26 14/6/26 15/6/26 16/6/26 17/6/26 FBC TWBC (4-11 times 10^9/L) — 8.25 — — — Hb ($11.5-16.5 \text{ g/100mL}$) — 10.6 — — — Platelet ($150-400 \times 10^9/\text{L}$) — 294 — — — BUSE / Renal Urea ($1.7-8.3 \text{ mmol/L}$) 9.5 12.9 13.5 15.1 — $\text{Na}^+$ ($135-145 \text{ mmol/L}$) — 137 136 143 — $\text{K}^+$ ($3.5-5.0 \text{ mmol/L}$) — 4.6 4.0 3.6 — $\text{Cl}^-$ ($96-106 \text{ mmol/L}$) — 97 96 99 — SCr ($64-122 \ \mu\text{mol/L}$) 149 136 136 151 — $\text{Ca}^{2+}$ ($2.1-2.6 \text{ mmol/L}$) — 2.21 — — — $\text{Mg}^{2+}$ ($0.7-1.3 \text{ mmol/L}$) — 0.99 — — — $\text{PO}_4^{3-}$ ($0.8-1.45 \text{ mmol/L}$) — 1.27 — — — eGFR — 35 — — — LFT Albumin ($35-50 \text{ g/L}$) — 26 — — — T.Bilirubin ($<20 \ \mu\text{mol/L}$) — 54.3 — — — T.Protein ($66-87 \text{ g/L}$) — 71 — — — ALP ($53-141 \text{ u/L}$) — 351 — — — ALT ($<32 \text{ u/L}$) — 7 — — — CE AST ($<37 \text{ u/L}$) — 37 — — — Others Urine PCR — 1.17 g/mmol — — — Date 14/6 15/6 16/6 17/6 Input 350 650 600 450 Ouput 950 1400 500 300 Balance -600 -750 +100 +150 14/6 Present to ED on 14/6 with Worsening failure symptoms Orthopnea Bilateral pitting edema Abdominal distension 14/6 10.50 am Currently: Less SOB Orthopnea Unable to lie flat On examination: alert BP: 138/83 mmHg PR: 94 SPO2: 98% DXT: 12.3 Lungs: Bilateral creps till M2 P/A: Thick abdomen, distended bilateral sacral + Breast edema CXR: Cardiomegaly with bilateral pleural effusion ECG: SR, Poor R wave progression Impression: Acute decompensated HF with underlying HFrEF Plan: Start IV Lasix 80 mg TDS IV Human albumin 20% 100 cc x 3/7 I/O Charting ROF 500 cc/day + low salt diet Daily RP monitoring (what is RP?) Start T. Dapagliflozin 10 mg OD (own med) T. Bisoprolol 5 mg OD Continue other own medicines Start T Valsartan 40 mg OD DXT QID S/C Mixtard 10/16 U BD S//C Clexane 40 mg OD (DVT prophylaxis) KIV MRA 15/6/26 8.35 am Currently: Under Room Air , less SOB, edema reducing On examination: alert, conscious BP: 118/76 mmHg PR: 68 Temp: 37 SPO2: 99% under room air I/O: 350/950=-600 Lungs: under a/e bilateral LL with crepitation (reducing compared to yesterday) Abdominal edema: reducing Bilateral pedal edema up to shin Impression: Acute decompensated HF with underlying HFrEF Plan: Continue IV Lasix 80 mg TDS with human albumin Strict I/O Charting ROF 500 cc/day + low salt diet Add T. Spironolactone 12.5 mg OD Take RP today To get new NPS date / CMRI date upon discharge DXT QID For COROS once able to lie flat 16/6 9.20 am Issue: Acute decompensated HF with underlying HFrEF Uncontrolled DM CKD Stage 3A Currently: Less SOB, orthopnea, generalised edema (reducing) On examination: not tachypneic BP: 140/72 mmHg PR: 61 Temp: 37 SPO2: 100% I/O: 650/1400/-750 Lungs: Bilateral LL crepts with under a/e Bilateral pedal edema up to shin with wrinkle signs (improving) Plan: Increase T. Spironolactone 25 mg OD Reduce IV Lasix 60 mg TDS + IV human albumin (continue 3/7) Strict I/O charting For COROS ULR? Off load / able to lie flat (aim thursday) Take RP today Change to basal bolus S/C actrapid 6 U TDS and S/C Inuslatard 18 U ON DXT QID # If BP permiasable and AKI improved KIV increase T. Valsartan 17/6 10 am Under room air, no more SOB BP unsupported ( meaning pls) Still have orthopnea No pedal edema Plan: T. Lasix 40 mg BD T. Spironolactone 12.5 mg BD T. Valsartan 40 mg BD For COROS if able to lie flat 18/6 10 am Issue: Acute decompensated HF with underlying HFrEF Currently: Under room air Unable to lie flat Orthopnea Still edematous O/E: alert, conscious , not tachypenic BP: 103/57 PR: 65 SPO2: 98% under room air Lungs: under a/e over bilateral LL + generalised edema (Improving) U/O: 450/300/+150 Plan: Continue off load For COROS once able to lie flat ROF 500 cc/day plus low salt diet IV lasix 40 mg TDS Medications given according to the mediation chart is: IV lasix 80 mg TDS given only at 8 am. 4 pm and 12 am not given T. empagliflozin 25 mg OD given everyday at 8 am from 14/6 till now T. spironolactone 12.5 mg OD given only at 16/6 8 am, then stopped. T. spironolactone 25 mg OD given on17/6 8 am and stopped S/C actrapid 6 units TDS S/C Insulatard 18 unit ON IV Lasix 60 mg tds given staRTING from 16/612 pm and 17/6 6 am and stopped T. spironolactone 12.5 mg BD given starting from 17/6 6 pm and continue on 18/6 8 am T. atorvastatin 40 mg ON from 14/6 till now T. glyprin 1/1 OD from 14/6 till now S/C clexane 40 mg OD fron 14/6 till now T.pantoprazole 40 mg OD from 14/6 till now IV lasix 80 mg TDS given from 14/6 till 16/6 and stopped IV human albumin 20% 100 cc OD x 3/7 given from 14/6 till 16/6 and stopped T. Bisoprolol 5 mg OD from 14/6 till now T. valsartan 40 mg OD from 14/6 till now …………………………………………………………………………………………………….. HOSPITAL SULTANAH BAHIYAH (Un-Official Report) Order ID RDIP00001240682 Order Category Radiology Order Type Ultrasonography Priority Urgent Patient Norsiah Binti Darus ,Female/64Y,ID:AS00908242 Encounter ID 16156001 Order Date Time 27/04/2026 08:36 Order Status Resulted - Complete Ordering Location Nursing Unit/CRW Ordering Practitioner Tan Jie Nee, DR Ordering Facility HOSPITAL SULTANAH BAHIYAH HOSPITAL SULTANAH Performing Facility BAHIYAH Order Format s/t Dr. Ong, granted U/S abdomen in patient USG abdomen TRO causes of abdominal distention + USG KUB TRO obstructive uropathy Underlying 1) DM - HbA1C July 2021: 8.2% - Under KK Simpang Kuala - on S/C Insulin & OHA 2) HPT 3) ?CKD stage 3A 4) IHD with HFrEF H/o admission in July 2021 for NSTEMI ECHO done on 4/2/26: ALL CHAMBER NORMAL SIZE MILD MR PR FLOW WITH PAEDP 12mmHg MILD TR WITH PASP 28mmHg NO AR/AS RWMA PRESENT-GLOBAL HYPOKINESIA LVEF 32% BY SIMPSON NO LV CLOT NO PERICARDIAL EFFUSION T Clinical Atorvastatin 40mg ON T Cardirpin 100mg OD T Bisoprolol 5mg OD S/C Mixtard 18/20 unit BD T Pantoprazole Comments 40mg OD T Spironolactone 25mg OM T Valsartan 40mg OD T Dapiga 10mg OD (self purchase) ============================= Admitted for 1. Symptomatic ascitis with under HFrEF 2. Congestive hepatopathy 3. AKI on CKD Tro obstructive uropathy breathlessness for x2/52 - worsening for x2/7 ABdominal distension x2/52 - gradually increasing LL swelling x2/52 Orthopnea + PND x2/7 PA: Soft non tender, generalised swelling, no mass palpable bedside scan done by Dr Tan CY (Cardio fellow): no ascitic fluid seen no tapping window Ur 11.3 -> 21:Cr 147 -> 278 AST 27 T. bili 21 -> 14 ALP 288-> 286 Reporting Practitioner : DRKANMANI2 Resulting Time : 30/04/2026 09:10 Event Date Time:30/04/2026 09:10 US Abdomen Abdomen performed on 30.04.2026. D1trasound ** Suboptimal study due to thick abdomen Findings: Liver appears homogenously increase in echogenicity with regular margin. No focal lesion. It measure s 16.5cm. No intrahepatic or extrahepatic ducts dilatation. Portal veins is patent with normal doppler flow: Gall bladder is well distended with thin wall. No gall bladder stones or sludge. No pericholecystic fluid collection. Visualised pancreas is normal. Spleen is normal with no focal lesion. It measures. 7.6cm. Both kiceys are normal in size and shape. However, both increase in echogenicity. Right kidney bipolar length = 8.3cm, PT = 0.8cm. Left kidney bipolar length = 10.1cm, PT = 1.1cm. No stones r hydronephrosis demonstrated bilaterally. No perinephric fluid collection. Urinary bladder is partially distended. No mass or calculus seen within. Visualised bilateral psoas muscles are normal. No mass or intraabdominal collection noted Free fluid noted at perihepatic and perisplenic region. Incidental finding: Right pleural effusion. Impressions: 1. Fatty liver with hepatomegaly. 2. Bilateral renal parenchymal disease. 3. Right pleural effusion and mild ascites. Exam Performed On 30/04/2026 08:06 By : DRJASONW2 - Jason Wong ,Dr Report Prepared On : 30/04/2026 09:10 By Radiologist : DRKANMANI2 - Kanmani, D Report Authorized On : 30/04/2026 09:10 By Radiologist : DRKANMANI2 - Kanmani, This is the previous report in april

Reading File
Now let me run parallel searches - medical library for HFrEF management, CPG Malaysia, and all relevant drug information.
Finding Sources
Finding Sources
Searching the Web

CPG Malaysia heart failure 2023 2024 guidelines HFrEF management treatment

Searching PubMed

"heart failure" AND "reduced ejection fraction" AND treatment guidelines

The CPG Malaysia 2023 (5th Ed) is confirmed. Let me now extract the full CPG content and relevant textbook sections in parallel.
Reading Web Page

https://www.moh.gov.my/images/04-penerbitan/penerbitan-klini…

Finding Sources
Finding Sources
Excellent. Now let me read the key textbook sections on HFrEF management and also search for specific drug information relevant to this case.
Reading File
Finding Sources
Finding Sources
Searching the Web

CPG Malaysia heart failure 2023 empagliflozin dapagliflozin SGLT2 valsartan ARB CKD stage 3 spironolactone dose recommendation

Reading File
Reading Web Page

https://www.moh.gov.my/images/04-penerbitan/penerbitan-klini…

I now have enough information to write comprehensive presentations. Let me also quickly search for COROS and NPS viability explanation.
Searching the Web

COROS coronary angiography CT cardiac viability study NPS nuclear perfusion scan heart failure ischemic cardiomyopathy Malaysia

I now have all the information needed. Let me compile both comprehensive scripts.---

COMPREHENSIVE CASE PREPARATION NOTES

Before the Scripts - Full Clinical Context You Must Know

KEY TERMINOLOGY EXPLAINED

COROS (Coronary CT Angiography / Invasive Coronary Angiography) In the Malaysian hospital context, "COROS" typically refers to Coronary Angiography - this may mean either:
  • CT Coronary Angiography (CTCA/CCTA): A non-invasive CT scan that visualizes the coronary arteries for blockages. It requires the patient to be able to lie flat and hold their breath briefly.
  • Invasive Coronary Angiography (ICA): A catheter-based procedure where contrast dye is injected directly into coronary arteries.
In this case, the plan says "For COROS once able to lie flat" - this strongly suggests CT coronary angiography (non-invasive, requires lying flat), used to rule out ischemic cause of her HFrEF. This patient has a known history of NSTEMI (July 2021), ECHO showing global hypokinesia with LVEF 32% - the purpose is to identify if her HFrEF is ischemic in origin and if coronary revascularization (PCI or CABG) would improve function.
NPS (Nuclear Perfusion Study / Myocardial Perfusion Scintigraphy) NPS is a nuclear imaging study (SPECT with Tc-99m or Thallium) that:
  • Assesses myocardial viability - identifies hibernating/stunned myocardium that may recover after revascularization
  • Differentiates ischemic vs non-ischemic segments
  • Helps determine if the globally hypokinetic heart has viable muscle that would benefit from PCI/revascularization
  • Patient with LVEF 32% + global RWMA - the question is: is there hibernating myocardium? If yes, PCI or CABG could improve LVEF.
KIV COROS +/- PCI = The team is planning to do a coronary angiogram; if significant coronary artery disease is found, PCI (percutaneous coronary intervention - stent) may be performed during the same sitting or in a separate procedure.
RP (Renal Profile) = Blood tests for kidney function: urea, creatinine, electrolytes (Na, K, Cl), eGFR. In a HF patient on diuretics, MRA, SGLT2i, this is monitored daily because:
  • Aggressive diuresis can worsen AKI
  • Spironolactone + ARB can raise potassium (hyperkalemia risk)
  • Valsartan can drop GFR
Ca-125 = 257 (normal <35 U/mL) CA-125 is a tumor marker classically associated with ovarian cancer. However, CA-125 is also significantly elevated in heart failure - congestion causes serosal inflammation (peritoneal, pleural membranes), which releases CA-125. A CA-125 of 257 in a patient with decompensated HF with ascites and pleural effusion is almost certainly explained by her cardiac failure rather than malignancy. The gynae referral and USG abdomen were done to rule out malignancy. The USG showed no abdominal mass, confirming HF as the likely cause. This is a known phenomenon - CA-125 correlates with degree of HF congestion and can serve as a marker of decongestion response.
BP Unsupported (17/6 note) = The BP recorded is without the support of vasopressors (i.e., the patient is maintaining their blood pressure on their own, without inotropes or vasopressors). It does NOT mean the BP is unmeasured. On 18/6, BP 103/57 - this is low but the patient is maintaining it without pharmacological support.

DISEASE UNDERSTANDING: HFrEF

Definition: HFrEF = Heart Failure with Reduced Ejection Fraction, defined as LVEF ≤40% (Malaysia CPG 2023, 5th Edition). This patient has LVEF 32% by Simpson's method.
Pathophysiology (Why? - the 7W framework):
WHO? 64-year-old Malay female with multiple comorbidities: DM, HPT, CKD Stage 3A, previous NSTEMI (July 2021), now with LVEF 32% and global RWMA.
WHAT? Acute Decompensated Heart Failure (ADHF) on top of chronic HFrEF. Presenting with worsening congestion: orthopnea, bilateral pitting edema, abdominal distension, bilateral creps.
WHY did she decompensate? Common precipitants (CHAMPION acronym from CPG Malaysia 2023):
  • C - Cardiac arrhythmia / Coronary events
  • H - Hypertension (uncontrolled)
  • A - Anemia (Hb 10.6 - mild anemia contributing)
  • M - Medication non-compliance (likely - she was on furosemide 40mg OD as outpatient, which was clearly insufficient)
  • P - Pulmonary causes (infection, PE)
  • I - Ischemia (history of NSTEMI)
  • O - Obesity / Obstructive sleep apnea
  • N - Non-cardiac (renal, thyroid)
In this case: likely medication non-adherence / inadequate outpatient diuresis (she was only on oral Lasix 40mg OD outpatient - clearly insufficient given degree of congestion), CKD-related fluid retention, hypoalbuminemia (albumin 26 g/L, normal 35-50) causing reduced oncotic pressure worsening edema, and congestive hepatopathy (ALP 351, high T.Bilirubin 54.3).
WHEN? Admitted 14/6/26, presenting over approximately 2 weeks of worsening symptoms.
WHERE? Hospital admission.
HOW? Mechanism: reduced cardiac output → neurohormonal activation (RAAS, sympathetic) → fluid retention → fluid redistribution → pulmonary congestion, peripheral edema, ascites.
WHAT HAPPENS if untreated? Cardiogenic shock, respiratory failure, death.

UNDERSTANDING KEY INVESTIGATIONS

TestThis PatientSignificance
LVEF 32% (ECHO 4/2/26)Severely reducedDefines HFrEF; drives all management decisions
Global RWMA (hypokinesia)PresentSuggests ischemic etiology (diffuse CAD) vs. dilated cardiomyopathy
Hb 10.6Mild anemiaAnemia worsens HF symptoms; may need investigation
Albumin 26 (low)HypoalbuminemiaReduces oncotic pressure; causes diuretic resistance; indication for albumin infusion
T.Bilirubin 54.3 (elevated)Congestive hepatopathyRight heart failure → hepatic venous congestion
ALP 351 (elevated)Cholestatic liver patternConsistent with congestive hepatopathy
SCr 136-151 (elevated)CKD Stage 3AeGFR 35 - guides drug dosing; risk of AKI with aggressive diuresis
Urea rising 12.9→13.5→15.1Worsening azotemiaCardiorenal syndrome type 1; monitor closely
Urine PCR 1.17Significant proteinuriaCKD + proteinuria; confirms renal parenchymal disease
ECG: Poor R wave progressionAnterior infarct patternConsistent with prior anterior NSTEMI
CXR: Cardiomegaly + bilateral pleural effusionPulmonary congestionConfirms decompensated HF

FLUID BALANCE INTERPRETATION

DayInputOutputBalanceInterpretation
14/6350950-600Good negative balance - diuresis working
15/66501400-750Excellent decongestion response
16/6600500+100Positive balance - concern, may indicate diuretic resistance or insufficient dose
17/6450300+150Continuing positive balance - not deconging adequately
The positive balance on 16/6-17/6 explains why IV Lasix was switched from 80mg TDS to 60mg TDS (step-down but still IV), and why furosemide dose needed re-evaluation. The patient was still orthopneic on 17-18/6.

MEDICATION ISSUES / PCI (Potential Clinical Issues) IDENTIFIED

PCI #1: IV Lasix 80mg TDS - only given at 8am; 4pm and 12am doses NOT administered
  • The medication chart shows IV Furosemide 80mg TDS was prescribed but only the morning dose (8am) was given - afternoon (4pm) and midnight (12am) doses were omitted.
  • This is a significant PCI. In acute decompensated HF, IV furosemide TDS means three doses per day, round the clock.
  • Missing two-thirds of the prescribed dose would significantly compromise decongestion.
  • This may explain the incomplete fluid removal and persistent congestion, and correlates with the positive balances on 16-17/6.
  • Recommendation: The nursing team should be notified; IV diuretics in ADHF must be administered as prescribed, including night-time doses.
PCI #2: Spironolactone dose and frequency inconsistency
  • 14/6 plan: "KIV MRA" (not started)
  • 15/6 plan: "Add T. Spironolactone 12.5mg OD"
  • Medication chart: Spiro 12.5mg OD given only on 16/6 8am, then stopped
  • 16/6 plan says: "Increase T. Spironolactone 25mg OD" - given 17/6 8am only
  • 17/6 plan: "T. Spironolactone 12.5mg BD"
  • Spiro 12.5mg BD given from 17/6 6pm and 18/6 8am
  • Issue: Inconsistent administration - doses not consistently given on 14-15/6. However, note that MRA was appropriately deferred until some decongestion was achieved, and K was monitored (K was 4.6 on 14/6, acceptable; 4.0 on 15/6, 3.6 on 16/6 - all within safe range for MRA).
PCI #3: Empagliflozin 25mg prescribed vs Dapagliflozin 10mg - DOSE DISCREPANCY
  • The plan on 14/6 says: "Start T. Dapagliflozin 10mg OD (own med)" - suggesting the patient self-purchases Dapagliflozin 10mg
  • The medication chart shows: "T. Empagliflozin 25mg OD given everyday at 8am from 14/6"
  • This is a PCI: Two different SGLT2 inhibitors, and empagliflozin 25mg was given instead of dapagliflozin 10mg.
    • The approved HF dose for empagliflozin is 10mg OD (EMPEROR-Reduced trial dose)
    • The approved HF dose for dapagliflozin is 10mg OD (DAPA-HF trial dose)
    • Empagliflozin 25mg is the higher glucose-lowering dose, NOT the HF indication dose
    • In acute decompensated HF, SGLT2 inhibitors should be used with caution - however, both ESC 2023 and CPG Malaysia 2023 support early initiation in HFrEF
    • The patient has CKD with eGFR 35 - dapagliflozin requires eGFR ≥30 (safe), empagliflozin requires eGFR ≥20 (safe at this eGFR)
    • Recommendation: Clarify which SGLT2i is being used; if empagliflozin, reduce to 10mg; if dapagliflozin 10mg as planned, continue
    • Also worth noting: in ADHF, SGLT2i initiation is safe and associated with better outcomes (EMPULSE trial)
PCI #4: IV Lasix dose stepping - appropriate
  • 80mg TDS → 60mg TDS (16/6) → 40mg TDS (18/6) → 40mg BD (oral, 17/6 plan)
  • Step-down was appropriate as patient showing some improvement in edema, but note she remained orthopneic.
PCI #5: Valsartan dose
  • Patient started on T. Valsartan 40mg OD (14/6), continued throughout
  • This is a low dose (target dose for HF is 160mg BD)
  • Appropriate to start low given CKD, rising urea/creatinine, and concurrent diuretic use
  • Note on 16/6: "If BP permissible and AKI improved, KIV increase T. Valsartan" - appropriate clinical decision-making
  • On 17/6: increased to T. Valsartan 40mg BD - appropriate step-up as BP was 118-140 and SCr stable
PCI #6: No ACE inhibitor - appropriate
  • Patient is on ARB (Valsartan), not ACE-I - this is appropriate. Per CPG Malaysia 2023, RAS blocker should be: ACEi OR ARB OR ARNI. The patient cannot be on ACEi + ARB simultaneously.
  • ARNI (Sacubitril/Valsartan / Entresto) would be the preferred upgrade over ARB alone - however, in acute setting, starting with ARB is acceptable with plan to upgrade to ARNI when stable.
PCI #7: No Clexane after 18/6?
  • SC Clexane 40mg OD from 14/6 - DVT prophylaxis appropriate in immobilized, hospitalized HF patient
  • Indicated: immobility + HF + CKD + elevated CA-125 (TRO malignancy)
  • Note: dose adjustment in CKD - standard DVT prophylaxis dose for CrCl <30 is 20mg OD; at CrCl/eGFR 35, Clexane 40mg OD is generally acceptable but some protocols suggest monitoring anti-Xa
PCI #8: Bisoprolol dose increase from 2.5mg → 5mg
  • Appropriate: patient was compensated enough on admission, heart rate 94, BP adequate
  • Beta-blockers should be continued in ADHF unless cardiogenic shock or bradycardia
  • On 18/6 with BP 103/57 and HR 65 - bisoprolol 5mg may need dose review

OVERALL MEDICATION RATIONALE TABLE

MedicationIndicationCPG Malaysia Recommendation
IV Furosemide 80mg TDS → 60mg TDS → 40mg TDSAcute decongestion in ADHFGrade I: Loop diuretics for symptomatic relief in ADHF; IV route for acute setting
IV Human Albumin 20% 100cc OD x 3/7Hypoalbuminemia (Albumin 26) causing diuretic resistanceGuideline-supported adjunct in hypoalbuminemic patients with diuretic resistance
T. Dapagliflozin 10mg OD (own med)HFrEF + DM - reduces HF hospitalization, CV mortalityGrade I: SGLT2i for all HFrEF regardless of diabetes status
T. Empagliflozin 25mg OD (dispensed)Discrepant from plan - see PCI #3 aboveHF dose should be 10mg
T. Bisoprolol 5mg ODHFrEF - proven mortality benefit; rate controlGrade I: Beta-blocker in all stable HFrEF
T. Valsartan 40mg OD/BDHFrEF - RAS blockade, reduce afterload and neurohormonal activationGrade I: ARB in HFrEF if ACEi not tolerated; dose to be titrated up
T. Spironolactone 12.5-25mg OD/BDHFrEF with NYHA II-IV + eGFR >30 + K <5.0Grade I: MRA in HFrEF; start low dose and titrate
SC Clexane 40mg ODDVT prophylaxis in immobilized hospitalized patientStandard of care in hospitalized medical patients
T. Atorvastatin 40mg ONDyslipidemia + IHD history (NSTEMI 2021); plaque stabilizationGrade I: Statin in IHD/HF with ischemic etiology
T. Glyprin (Aspirin 100mg) ODSecondary prophylaxis post-NSTEMI; antiplateletGrade I: Antiplatelet for IHD
T. Pantoprazole 40mg ODGastroprotection with aspirin useAppropriate: PPI co-prescription with antiplatelet
SC Actrapid 6U TDS + Insulatard 18U ONUncontrolled DM (DXT 12.3)Appropriate: Basal-bolus insulin for inpatient DM management
SC Mixtard 18/20U BD (home)Outpatient DM controlChanged to basal-bolus as inpatient for better control

DRUGS NOT GIVEN BUT WORTH DISCUSSING

ARNI (Sacubitril/Valsartan / Entresto)
  • CPG Malaysia 2023 Recommendation: ARNI is the PREFERRED RAS blocker over ACEi or ARB alone in HFrEF (Grade I, A).
  • Reduces HF hospitalization and CV mortality more than ARBs.
  • Can be started de novo at 24/26mg BD in the acute setting.
  • Why not used here? May be cost-related (not funded), or the team preferred to stabilize first. Could be flagged as a suggestion: "Is there a plan to upgrade to ARNI (Sacubitril/Valsartan) on follow-up per CPG Malaysia 2023 recommendation?"
Ivabradine
  • Consider if HR remains ≥70 bpm in sinus rhythm despite maximum tolerated beta-blocker, with LVEF ≤35%.
  • Not currently indicated as HR is controlled (68 bpm on 15/6).
Vericiguat
  • Consider in worsening HF despite GDMT following hospitalization.
  • Not yet indicated as first-line.
Hydralazine + Isosorbide Dinitrate (H-ISDN)
  • Alternative to RAS blockers if ACEi/ARB/ARNI not tolerated (e.g., renal failure, hyperkalemia).
  • Not needed currently as ARB is tolerated.

SCRIPT TYPE 1: CP2 FORM FLOW (Problem → Medication → Indication → Appropriateness)

PRESENTATION SCRIPT 1: CP2-BASED FORMAT

"Good morning/afternoon. My name is [Your Name], and I will be presenting the case of Madam NS."

1. PATIENT DEMOGRAPHICS

"The patient is Madam NS, a 64-year-old Malay female, currently admitted to the cardiology ward."

2. CHIEF COMPLAINT

"She presented to the emergency department on 14th June 2026 with complaints of:
  • Worsening heart failure symptoms over the preceding two weeks - specifically worsening shortness of breath, orthopnea (inability to lie flat), bilateral pitting edema, and abdominal distension."

3. DIAGNOSIS

"Her working diagnosis is Acute Decompensated Heart Failure (ADHF) with underlying Heart Failure with Reduced Ejection Fraction (HFrEF), with an LVEF of 32% documented on ECHO dated 4th February 2026 showing global hypokinesia and regional wall motion abnormalities."
"She has the following underlying comorbidities:
  • Type 2 Diabetes Mellitus - on subcutaneous insulin
  • Hypertension
  • Chronic Kidney Disease Stage 3A (eGFR 35, SCr 136)
  • Ischemic Heart Disease with history of NSTEMI in July 2021
  • Congestive Hepatopathy - elevated ALP 351, T.Bilirubin 54.3, albumin low at 26
  • Hypoalbuminemia - albumin 26 g/L (normal 35-50)"
"Her ECHO also showed mild mitral regurgitation, mild tricuspid regurgitation with a pulmonary artery systolic pressure of 28 mmHg, and no LV clot or pericardial effusion."
"She is under investigation to rule out ischemic etiology for her HFrEF. A Nuclear Perfusion Study (NPS) was planned to assess myocardial viability - that is, to determine whether her globally hypokinetic myocardium contains hibernating or stunned segments that could recover function after revascularization. A COROS (coronary angiography) was also planned to visualize her coronary arteries for significant stenosis, with a view to PCI if suitable lesions are found. This requires the patient to be able to lie flat, which has been a limiting factor given her ongoing orthopnea."

4. DAY-BY-DAY FLOW

DAY 1 - 14th June 2026

"On Day 1 of admission, Madam NS presented with active heart failure decompensation. Her clinical findings were: BP 138/83 mmHg, PR 94, SpO2 98%, DXT 12.3 mmol/L. Lungs had bilateral crepitations up to the middle zone. CXR showed cardiomegaly with bilateral pleural effusion. ECG showed sinus rhythm with poor R wave progression - consistent with her prior anterior NSTEMI."
"The clinical impression was Acute Decompensated Heart Failure with underlying HFrEF."
The following medications were initiated or continued on Day 1:
1. IV Furosemide (Lasix) 80mg TDS
"Madam NS was started on IV Furosemide 80mg three times daily for the indication of acute decompensated heart failure with signs of severe fluid overload - bilateral pleural effusion, bilateral pitting edema, abdominal distension, and bilateral crepitations to mid-zone bilaterally. Loop diuretics are the cornerstone of treatment in ADHF, relieving pulmonary and systemic congestion. Per CPG Malaysia Management of Heart Failure 2023 (5th Edition), IV loop diuretics are recommended as the initial step in symptomatic fluid overload (Grade I). IV administration is preferred over oral in acute settings due to more reliable and rapid absorption. The dose of 80mg TDS represents an appropriate escalation from her outpatient dose of Lasix 40mg OD."
"However, a Potential Clinical Issue (PCI) was identified: Upon review of the medication administration chart, the 8am dose of IV Furosemide 80mg was administered, but the 4pm and 12am doses were NOT given throughout the initial days of admission. This represents omission of two out of three prescribed doses - effectively negating much of the intended diuretic effect. This is clinically significant as it may explain the incomplete decongestion seen on days 3 and 4 (positive fluid balance of +100 and +150 on 16/6 and 17/6). This should be flagged to the ward nursing team."
2. IV Human Albumin 20% 100cc OD x 3/7
"Madam NS was started on IV Human Albumin 20% (100cc once daily for 3 days, from 14/6 to 16/6) for the indication of hypoalbuminemia with diuretic resistance in the context of ADHF. Her serum albumin was found to be critically low at 26 g/L (normal 35-50 g/L). Hypoalbuminemia reduces oncotic pressure, shifting fluid from the intravascular space into the interstitial and third spaces - causing edema while paradoxically reducing effective circulating volume. This renders loop diuretics less effective because furosemide is highly protein-bound; low albumin means less drug reaches the tubular lumen. The strategy of albumin infusion prior to or concurrent with furosemide in hypoalbuminemic patients is supported by evidence showing improved diuretic response and faster decongestion. This is a clinically appropriate intervention in this patient."
3. T. Dapagliflozin 10mg OD (patient's own medication)
"Per the doctor's plan, T. Dapagliflozin 10mg OD (patient's self-purchased medication) was to be continued. Dapagliflozin is an SGLT2 inhibitor indicated for HFrEF (regardless of diabetic status) to reduce the risk of cardiovascular death and HF hospitalization. This is a Foundational HF Medication per CPG Malaysia 2023, with a Grade I, Level A recommendation. The DAPA-HF trial demonstrated a significant 26% reduction in worsening HF events and CV mortality with dapagliflozin 10mg OD."
"PCI: However, a discrepancy was found. The medication administration chart shows that the patient was actually dispensed and administered T. Empagliflozin 25mg OD (not Dapagliflozin 10mg). Furthermore, the dose of 25mg is the higher glycemic-control dose of empagliflozin - the approved heart failure dose for empagliflozin is 10mg OD (as established in the EMPEROR-Reduced trial). Both dapagliflozin 10mg and empagliflozin 10mg have Class I recommendations for HFrEF. However, empagliflozin 25mg has not been studied in HF - only the 10mg dose carries the HF indication. This dose should be reviewed and corrected to either the intended dapagliflozin 10mg or empagliflozin 10mg. Regarding safety in CKD: dapagliflozin is approved down to eGFR ≥30 ml/min/1.73m², and empagliflozin down to ≥20 ml/min/1.73m² - this patient's eGFR of 35 is safe for both agents."
4. T. Bisoprolol 5mg OD (increased from 2.5mg OD)
"Madam NS's outpatient bisoprolol was increased from 2.5mg OD to 5mg OD from Day 1 of admission. Bisoprolol is a cardioselective beta-1 blocker, indicated as a Foundational HF Medication for HFrEF per CPG Malaysia 2023 (Grade I). Beta-blockers reduce sympathetic overactivation in HF, decrease heart rate, reduce ventricular remodeling, and reduce mortality. The three beta-blockers with proven mortality benefit in HFrEF are bisoprolol, carvedilol, and metoprolol succinate. Bisoprolol is the preferred choice in this patient given her CKD (hepatic metabolism, renal excretion of active metabolite is minimal). The dose increase from 2.5mg to 5mg OD is appropriate given the patient's heart rate was 94 on admission and BP was adequate at 138/83. Per CPG Malaysia 2023, beta-blockers should be continued during ADHF unless the patient is in cardiogenic shock or has hemodynamic instability."
5. T. Valsartan 40mg OD (newly started)
"Madam NS was started on T. Valsartan 40mg OD on Day 1 of admission. Valsartan is an Angiotensin Receptor Blocker (ARB), indicated as a RAS blocker under the Foundational HF Medications for HFrEF per CPG Malaysia 2023 (Grade I). ARBs block the AT1 receptor, reducing aldosterone secretion, vasodilation, and reducing ventricular remodeling. In HFrEF, the preferred RAS blocker hierarchy per CPG Malaysia 2023 is: ARNI > ACEi > ARB. This patient was started on an ARB rather than ARNI, which is acceptable - particularly given the acute setting, CKD, and need to first establish tolerability. A starting dose of 40mg OD is appropriate (target dose is 160mg BD; low starting dose is prudent given her CKD and concurrent diuretic therapy). The plan on 16/6 to increase if BP and renal function permit shows appropriate titration strategy. Worth discussing: A plan to upgrade to ARNI (Sacubitril/Valsartan / Entresto) at follow-up should be considered per CPG Malaysia 2023, given ARNI has superior outcomes compared to ARB alone in HFrEF."
6. SC Clexane (Enoxaparin) 40mg OD
"Subcutaneous Clexane 40mg OD was started on Day 1 for DVT prophylaxis in a hospitalized, immobilized patient with HF. This is appropriate standard of care. In the context of this admission, Clexane is doubly indicated given: (1) immobility from severe fluid overload, (2) active malignancy query (Ca-125 elevated at 257 U/mL). Note: at eGFR 35, the standard prophylactic dose of 40mg OD is generally acceptable. Some guidelines suggest a dose reduction to 20mg OD for eGFR <30 - at eGFR 35, 40mg OD remains within safe prescribing."
7. SC Mixtard 18/20 units BD (continued, later changed)
"The patient's outpatient insulin regime - SC Mixtard (pre-mixed insulin: 30% soluble + 70% isophane) 18 units AM / 20 units PM BD - was initially continued. However, on Day 3 (16/6), this was appropriately switched to a basal-bolus regimen: SC Actrapid 6U TDS (bolus) and SC Insulatard 18U ON (basal). The switch is clinically appropriate for an inpatient with uncontrolled DM (DXT 12.3 on admission) as the basal-bolus regimen allows better glycemic control with dose titration based on DXT monitoring QID. Pre-mixed insulin is less flexible for inpatient use."
8. T. Atorvastatin 40mg ON (continued from outpatient)
"Atorvastatin 40mg once nightly was continued from the patient's outpatient regime. The indication is secondary prevention in Ischemic Heart Disease (post-NSTEMI 2021) and dyslipidemia. Per CPG Malaysia on Stable Coronary Artery Disease and ACS guidelines, a high-intensity statin is indicated in all patients with established IHD. Atorvastatin 40mg is a moderate-to-high intensity statin. Note: In this patient with congestive hepatopathy (elevated ALP 351, T.Bilirubin 54.3), LFT monitoring is advisable. AST was 37 (upper limit of normal), ALT was 7 (normal) - statin use is acceptable as there is no significant transaminitis."
9. T. Glyprin (Aspirin) 100mg OD (continued from outpatient)
"Aspirin 100mg OD was continued. The indication is secondary antiplatelet prophylaxis in established IHD with prior NSTEMI (July 2021). Per CPG Malaysia ACS guidelines and Stable CAD guidelines, long-term aspirin (75-100mg OD) is recommended for secondary prevention post-ACS. This is clinically appropriate."
10. T. Pantoprazole 40mg OD (continued from outpatient)
"Pantoprazole 40mg OD was continued for the indication of gastroprotection in a patient on long-term aspirin. Proton pump inhibitor co-prescription with antiplatelet therapy is standard of care to reduce the risk of gastrointestinal bleeding. This is clinically appropriate."
"MRA (Spironolactone) was deferred on Day 1 (documented as KIV MRA). This is appropriate - in ADHF, initiation of MRA should be deferred until some decongestion is achieved, potassium is acceptable (K was 4.6 on 14/6 - borderline), and renal function is monitored. Additionally, concurrent ACE/ARB + MRA increases hyperkalemia risk - appropriate to monitor RP first."

DAY 2 - 15th June 2026

"On Day 2, Madam NS showed improvement - less SOB, crepitations reducing, abdominal edema reducing. BP 118/76, PR 68, SpO2 99% on room air. Fluid balance was -600ml (14/6) then -750ml (15/6). Input/output charting confirms response to diuresis."
New addition: T. Spironolactone 12.5mg OD
"On Day 2, T. Spironolactone 12.5mg OD was added. Spironolactone is a Mineralocorticoid Receptor Antagonist (MRA) - one of the Foundational HF Medications per CPG Malaysia 2023. The indication is HFrEF with symptomatic heart failure (NYHA Class III-IV) to reduce morbidity and mortality. The RALES trial demonstrated that spironolactone reduced all-cause mortality by 30% in severe HFrEF. Prerequisites for use: eGFR >30 (patient's eGFR is 35 - meets criteria), K <5.0 mmol/L (patient's K was 4.0 on 15/6 - appropriate), no significant renal impairment (SCr 136 - acceptable). A starting dose of 12.5mg OD is appropriate given her CKD Stage 3A. Target dose is 25-50mg OD. Per CPG Malaysia 2023: MRA is recommended for all HFrEF NYHA II-IV with eGFR >30 and K <5.0."
"PCI regarding Spironolactone administration: The medication chart reveals that spironolactone 12.5mg OD was only given on 16/6 at 8am (not 15/6 as planned when it was added), then stopped after one dose. There appears to be a delay in administration and inconsistent administration. Monitoring of renal profile before and after initiation is warranted."

DAY 3 - 16th June 2026

"On Day 3, Madam NS had persistent bilateral crepitations and bilateral pedal edema to the shin, but edema was reducing (wrinkle signs noted - a clinical marker of improving pedal edema). However, fluid balance became positive (+100ml). BP 140/72, PR 61."
Changes on Day 3:
1. Spironolactone increased to 25mg OD "Spironolactone was increased from 12.5mg to 25mg OD on Day 3. This titration is appropriate given K was 4.0 on 15/6 (safe for uptitration) and the patient had NYHA Class III symptoms. However, RP monitoring (K and SCr) should accompany this step."
2. IV Furosemide reduced to 60mg TDS + continued Human Albumin "IV Furosemide was reduced from 80mg TDS to 60mg TDS on Day 3. This step-down was made given some clinical improvement (reducing edema, improving crepitations). Human albumin 20% was continued (third day of the 3-day course). This is appropriate - albumin infusion helps maintain oncotic pressure while diuresis continues."
3. Insulin changed to basal-bolus regimen "As discussed, the premixed Mixtard was switched to SC Actrapid 6U TDS + SC Insulatard 18U ON for better inpatient glycemic control."
4. Plan to increase Valsartan if BP permissible and AKI improved "The team noted that Valsartan could be uptitrated when BP and renal function permit. This demonstrates appropriate sequential titration strategy as per CPG Malaysia 2023 - avoid uptitrating multiple agents simultaneously."

DAY 4 - 17th June 2026

"On Day 4, Madam NS had no more SOB, no pedal edema. BP was described as 'unsupported' - meaning she was maintaining her blood pressure without vasopressors. Still had orthopnea. Fluid balance remained marginally positive (+150ml on 17/6)."
Changes on Day 4:
1. IV Furosemide 60mg TDS → planned transition to T. Lasix 40mg BD (oral) "The plan on 17/6 was to transition to T. Lasix 40mg BD (oral). This represents a step-down from IV to oral diuretic, appropriate as the patient was improving clinically. However, this should be guided by fluid balance - with still positive balance, clinical judgment is needed."
2. Spironolactone 12.5mg BD "Spironolactone was changed to 12.5mg BD (25mg/day total) - equivalent in daily dose to the 25mg OD prescribed on Day 3, but split into twice-daily dosing. This is acceptable."
3. Valsartan 40mg BD "Valsartan was increased to 40mg BD (from 40mg OD). This doubling of the daily dose is appropriate given BP was 118-140 systolic and some clinical improvement, though creatinine was rising (151 on 16/6). Close monitoring of renal profile is essential with this uptitration."

DAY 5 - 18th June 2026

"On Day 5, Madam NS was still under room air, unable to lie flat, orthopneic. BP dropped to 103/57 mmHg. Still edematous. Fluid balance positive (+150ml on 17/6). Lungs: reduced air entry bilateral lower lobes with generalized edema."
Changes on Day 5:
"IV Lasix 40mg TDS was restarted - this reflects that the oral diuretic was insufficient given persistent congestion. BP of 103/57 is concerning:"
  • "Bisoprolol 5mg may need review given hypotension"
  • "Valsartan 40mg BD dose needs monitoring - ARB causes vasodilation and can lower BP further"
  • "Low BP limits uptitration of other agents"
  • "The team should ensure the COROS is planned once the patient can lie flat - this is critical for determining whether revascularization can improve her cardiac function"

5. OVERALL - PCI SUMMARY / NO PCI (if none found)

"Overall, several Potential Clinical Issues were identified in this admission:"
  1. PCI 1 - Omission of IV Furosemide TDS doses: The 4pm and 12am doses of IV Furosemide 80mg TDS were not administered on multiple days. This is a significant medication administration error that likely contributed to incomplete decongestion and positive fluid balance on days 3-4. Recommendation: Full TDS dosing must be maintained; night doses are critical in ADHF management.
  2. PCI 2 - Empagliflozin 25mg dispensed instead of Dapagliflozin 10mg: The plan documented Dapagliflozin 10mg (patient's own), but the chart shows Empagliflozin 25mg was given. The 25mg dose has no indication for heart failure - only 10mg is approved for HF. This should be corrected to empagliflozin 10mg or dapagliflozin 10mg.
  3. PCI 3 - Inconsistent spironolactone administration: Spironolactone doses were inconsistently given, with several omitted doses identified on the medication chart. Regular administration of MRA is necessary to achieve mortality and morbidity benefits in HFrEF.
  4. PCI 4 - Upgrade to ARNI not discussed: Per CPG Malaysia 2023, ARNI (Sacubitril/Valsartan) is the preferred RAS blocker in HFrEF over ARB alone. This patient is currently on Valsartan ARB. While appropriate for the acute phase, a plan to upgrade to ARNI at clinic follow-up should be documented and discussed.
  5. Observation on COROS: The patient has not yet undergone COROS as she is unable to lie flat due to orthopnea. This is a critical pending investigation - the coronary anatomy will determine if she has ischemic HFrEF amenable to revascularization, which could potentially improve her LVEF.

6. THANK YOU

"In summary, this is a case of a 64-year-old lady with multiple comorbidities who was admitted for acute decompensated HFrEF. The management followed the CPG Malaysia Heart Failure 2023 guidelines with initiation of Foundational HF Medications - SGLT2i, ARB, beta-blocker, MRA - alongside aggressive decongestion with IV furosemide and albumin infusion. Several PCIs were identified relating to medication administration errors and one potential drug-dose discrepancy. The patient is being planned for COROS once she can lie flat, to assess for ischemic etiology and potential revascularization. Thank you."

SCRIPT TYPE 2: STORYTELLING FORMAT (Diagnosis → Then Medications)

PRESENTATION SCRIPT 2: STORYTELLING FORMAT

"Good morning/afternoon. My name is [Your Name], and today I will be presenting the case of Madam NS, a 64-year-old Malay female."

1. PATIENT AND CHIEF COMPLAINT

"Madam NS is a 64-year-old Malay female with a background of Type 2 Diabetes Mellitus, Hypertension, Chronic Kidney Disease Stage 3A, and Heart Failure with Reduced Ejection Fraction (HFrEF) currently under investigation to rule out ischemic etiology. She also has a history of a Non-ST Elevation Myocardial Infarction (NSTEMI) in July 2021."
"She was brought to the Emergency Department on the 14th of June 2026 with a chief complaint of worsening heart failure symptoms - specifically progressive shortness of breath, orthopnea, bilateral pitting edema, and abdominal distension over the preceding two weeks, worsening in the last two days prior to admission."

2. DIAGNOSIS

"Based on her clinical presentation, investigations, and prior echocardiographic data, Madam NS was diagnosed with Acute Decompensated Heart Failure superimposed on her known HFrEF with an LVEF of 32%."
"To give you some background - her ECHO performed on 4th February 2026 showed: LVEF 32% by Simpson's method, global hypokinesia with regional wall motion abnormalities, mild mitral and tricuspid regurgitation, and a pulmonary artery systolic pressure of 28 mmHg. No LV clot, no pericardial effusion."
"On examination at 10:50am on Day 1: BP was 138/83, PR 94, SpO2 98%, DXT 12.3. Lungs had bilateral crepitations to the middle zone bilaterally. Abdomen was distended with bilateral sacral and breast edema. Her CXR confirmed cardiomegaly with bilateral pleural effusion. ECG showed sinus rhythm with poor R wave progression - consistent with her prior anterior ischemic insult."
"Her laboratory profile showed a markedly low albumin of 26 g/L (normal 35-50), contributing to diuretic resistance and anasarca. Her serum creatinine was elevated at 136 μmol/L (eGFR 35) consistent with CKD Stage 3A. Liver function tests showed elevated ALP 351, total bilirubin 54.3, and AST 37 - this picture of cholestatic hepatopathy is consistent with congestive hepatopathy from right heart failure. Her hemoglobin was 10.6 g/dL - mild anemia, which may worsen HF symptoms."
"She was also noted to have urine PCR of 1.17 g/mmol - reflecting significant proteinuria from her underlying bilateral renal parenchymal disease seen on USG abdomen performed in April 2026."
"It is worth explaining her investigative plan: A Nuclear Perfusion Study (NPS/viability study) was planned to assess whether her globally hypokinetic myocardium contains hibernating or stunned viable segments that might recover function after revascularization. This is critical because if significant viable myocardium exists, revascularization via COROS (coronary angiography) and potentially PCI (percutaneous coronary intervention) could improve her LVEF and outcomes. The COROS requires the patient to be able to lie flat - which has been the limiting factor in this admission, as she remains orthopneic."

3. TREATMENT NARRATIVE - DAY BY DAY

DAY 1 - 14th June 2026: Initiating Decongestion and Foundational HF Therapy

"With a diagnosis of Acute Decompensated Heart Failure with underlying HFrEF, the medical team immediately began aggressive decongestion and initiated guideline-directed medical therapy."
"Madam NS was commenced on IV Furosemide (Lasix) 80mg three times daily. Furosemide is a loop diuretic that acts on the thick ascending limb of the Loop of Henle, inhibiting the Na-K-2Cl co-transporter, thereby promoting natriuresis and diuresis. In the setting of ADHF with severe fluid overload, intravenous loop diuretics are the cornerstone of treatment, as they bypass oral bioavailability issues and provide faster and more predictable diuresis. Per CPG Malaysia Management of Heart Failure 2023, IV loop diuretics carry a Grade I recommendation for symptomatic relief in ADHF. The dose of 80mg TDS represents an appropriate dose escalation - three times the patient's outpatient oral dose of 40mg OD - to overcome the diuretic resistance that commonly accompanies decompensation."
"Alongside diuretics, IV Human Albumin 20% 100cc once daily for three days was started. Madam NS's albumin was critically low at 26 g/L. In states of hypoalbuminemia, oncotic pressure falls, water shifts to the interstitial space, and the effective circulating volume contracts - paradoxically worsening edema while the kidneys perceive volume depletion. Additionally, furosemide is 98% protein-bound; low albumin reduces tubular delivery and diuretic efficacy. Albumin infusion corrects oncotic pressure, augments the diuretic effect, and improves intravascular volume. This is a clinically appropriate and evidence-supported adjunct strategy in hypoalbuminemic ADHF patients."
"Turning to the Foundational HF Medications - per CPG Malaysia 2023, all four classes should ideally be initiated or continued before or at discharge. On Day 1:"
"T. Bisoprolol was increased from 2.5mg OD to 5mg OD. Bisoprolol is a cardioselective beta-1 adrenergic blocker - one of only three beta-blockers with proven mortality benefit in HFrEF (alongside carvedilol and metoprolol succinate). Its role in HFrEF is to blunt the harmful neurohormonal sympathetic overactivation, reduce heart rate, and allow favorable ventricular remodeling. The CIBIS-II trial established a 34% reduction in all-cause mortality with bisoprolol in HFrEF. In this admission, with HR of 94 and adequate BP, increasing bisoprolol from 2.5mg to 5mg OD is appropriate. Beta-blockers should be continued during ADHF unless cardiogenic shock, hemodynamic instability, or severe bradycardia is present - none of which apply here."
"T. Valsartan 40mg OD was newly initiated. Valsartan is an Angiotensin Receptor Blocker (ARB) - a Renin-Angiotensin-Aldosterone System (RAAS) blocker that antagonizes the AT1 receptor, reducing aldosterone secretion, reducing afterload, preventing neurohormonal-driven cardiac remodeling, and improving clinical outcomes in HFrEF. Per CPG Malaysia 2023, the preferred RAS blocker is ARNI, followed by ACEi, then ARB. Valsartan was chosen as it is cost-accessible and appropriate for this patient who requires titration. The starting dose of 40mg OD is appropriate given her CKD and concurrent diuretic therapy. The target dose is 160mg BD, to be uptitrated as tolerated."
"T. Dapagliflozin 10mg OD (patient's own medication) was to be continued - and in the medication chart, T. Empagliflozin 25mg OD was administered. Both dapagliflozin and empagliflozin are SGLT2 inhibitors (SGLT2i) - the newest class of Foundational HF Medications. SGLT2i act on the proximal renal tubule, inhibiting glucose and sodium reabsorption, resulting in glycosuria, natriuresis, and a mild osmotic diuresis. Beyond glycemic control, SGLT2i have pleiotropic cardiac effects: they reduce preload and afterload, decrease sympathetic tone, have anti-fibrotic and anti-inflammatory properties, and appear to reduce myocardial metabolic stress. The DAPA-HF trial (dapagliflozin 10mg) and EMPEROR-Reduced trial (empagliflozin 10mg) both demonstrated significant reductions in HF hospitalization and CV mortality in HFrEF regardless of diabetic status - Grade I, Level A recommendation in CPG Malaysia 2023. However, a PCI exists: empagliflozin was given at 25mg - this is the higher diabetes dose, not the 10mg HF-approved dose. The dose should be reviewed and corrected to 10mg."
"MRA was deferred on Day 1 (documented as KIV MRA). This is appropriate - MRA initiation in ADHF should be approached cautiously given risk of hyperkalemia (K was 4.6 on admission, borderline elevated), and the team correctly opted to wait for decongestion and RP monitoring."
"The patient's outpatient medications - Atorvastatin 40mg ON, Aspirin (Glyprin) 100mg OD, and Pantoprazole 40mg OD - were continued. Atorvastatin is a high-potency HMG-CoA reductase inhibitor for secondary prevention of cardiovascular events in her established IHD (post-NSTEMI). Aspirin 100mg OD is an antiplatelet agent for secondary prevention post-NSTEMI, with lifelong indication. Pantoprazole 40mg OD is a proton pump inhibitor prescribed for gastroprotection in a patient on long-term aspirin, reducing the risk of upper GI bleeding."
"SC Clexane (Enoxaparin) 40mg OD was started for DVT prophylaxis - standard of care in a hospitalized, immobilized, medically unwell patient. DVT risk is elevated in decompensated HF with reduced mobility and venous stasis."
"DXT QID monitoring and SC Mixtard 18/20U BD (then later switched to basal-bolus) were continued for DM management."

DAY 2 - 15th June 2026: Partial Response - Adding MRA

"By Day 2, Madam NS showed clinical improvement: less SOB, crepitations reducing, edema reducing. PR had fallen from 94 to 68. Fluid balance was negative at -600ml (Day 1) and -750ml (Day 2) - confirming adequate diuretic response."
"T. Spironolactone 12.5mg OD was added. Now that the patient had demonstrated adequate diuresis, K had fallen to 4.0 mmol/L, and SCr was 136 (eGFR 35), the team appropriately initiated spironolactone as the MRA (Mineralocorticoid Receptor Antagonist) - the third Foundational HF Medication. Spironolactone blocks aldosterone's action on the mineralocorticoid receptor in the distal tubule, reducing sodium retention, potassium excretion, and myocardial fibrosis. The RALES trial proved a 30% reduction in mortality in severe HFrEF with spironolactone. Per CPG Malaysia 2023, MRA is recommended in HFrEF with NYHA II-IV, eGFR >30 and K <5.0 (Grade I). The starting dose of 12.5mg OD is appropriate in the context of CKD Stage 3A."
"The plan was also made to obtain a new NPS (Nuclear Perfusion Study) date and CMRI (Cardiac MRI) date upon discharge - reflecting ongoing investigation for ischemic vs. non-ischemic HFrEF etiology."

DAY 3 - 16th June 2026: Plateau - Dose Adjustment

"On Day 3, edema was reducing (wrinkle signs noted over pedal region - a positive prognostic sign). However, fluid balance became positive at +100ml - signaling a plateau in decongestion, likely partly attributable to the missed TDS doses of IV furosemide."
"Spironolactone was increased to 25mg OD. Given K was 3.6 (Day 3, 16/6) - well within safe range - the MRA was uptitrated. The standard maintenance dose for spironolactone in HFrEF is 25-50mg OD."
"IV Furosemide was reduced to 60mg TDS - a step-down reflecting partial clinical improvement. Human albumin infusion continued (completing the 3-day course)."
"Insulin was switched to basal-bolus regimen (Actrapid 6U TDS + Insulatard 18U ON) for better inpatient glycemic management, replacing the less flexible premixed Mixtard."
"The note also states: 'If BP permissible and AKI improved, KIV increase Valsartan' - this reflects cautious sequential dose escalation per guidelines, ensuring renal function is not compromised before uptitrating."

DAY 4 - 17th June 2026: Planning Transition to Oral Therapy

"On Day 4, Madam NS had no more SOB, no pedal edema. Still orthopneic. Fluid balance marginally positive (+150ml)."
"Plan to transition to T. Lasix 40mg BD (oral) from IV - appropriate step-down when clinical improvement is evident. However, given positive balance and persistent orthopnea, this required close monitoring."
"Spironolactone was changed to 12.5mg BD (equivalent to 25mg/day but split into twice-daily dosing - generally acceptable; some evidence suggests BD dosing may provide more consistent mineralocorticoid blockade)."
"Valsartan was increased to 40mg BD - appropriate uptitration step given BP was 118-140 systolic range during the preceding days and some clinical improvement."

DAY 5 - 18th June 2026: Persistent Congestion - Step Back Up

"By Day 5, Madam NS remained orthopneic and unable to lie flat. BP dropped to 103/57 mmHg. Still had generalized edema. Fluid balance was positive."
"The BP drop is a concern - it may reflect the combined vasodilatory effect of Valsartan 40mg BD, the effects of persistent fluid depletion from diuresis, and the underlying reduced cardiac output of HFrEF. IV Furosemide 40mg TDS was restarted - reflecting the team's clinical judgment that oral diuresis was inadequate."
"At this BP, careful monitoring of the bisoprolol dose (5mg OD) and valsartan (40mg BD) is warranted. Per CPG Malaysia 2023, if SBP falls below 90-100mmHg, dose reduction of beta-blockers and RAS blockers should be considered, while MRA and SGLT2i can usually be maintained as they have minimal hemodynamic effects."
"COROS remains deferred as the patient still cannot lie flat due to orthopnea. The coronary angiogram is critical for the next step in management."

4. PCIs (POTENTIAL CLINICAL ISSUES)

"During my review of this admission, I have identified the following Potential Clinical Issues:"
PCI 1 - IV Furosemide 80mg TDS: Doses omitted from administration chart "IV Furosemide 80mg TDS was prescribed but only the 8am dose was administered on multiple days; the 4pm and 12am doses were not given. This represents omission of 2/3 of the intended diuretic dose. In ADHF, round-the-clock IV diuretic dosing is essential for continuous decongestion. The positive fluid balance on days 3-4 may be attributable in part to this omission. This should be escalated to the nursing team and documented."
PCI 2 - Empagliflozin 25mg instead of Dapagliflozin 10mg "The prescription plan documented Dapagliflozin 10mg (patient's own medication), but the medication chart shows Empagliflozin 25mg OD was administered. Empagliflozin 25mg is the glucose-lowering dose, not the approved HF dose. For heart failure, empagliflozin is approved at 10mg OD (EMPEROR-Reduced, 2021). The dose should be reviewed and corrected. The prescriber should confirm the intended agent and dose."
PCI 3 - Spironolactone administration inconsistency "Spironolactone was prescribed but not administered on the date it was planned to start (15/6), with only a single dose given on 16/6, then another dose change on 17/6. Consistent administration is necessary for therapeutic benefit. RP should be checked 48-72 hours after initiation."
PCI 4 - ARNI not planned for discharge/follow-up "Per CPG Malaysia 2023, ARNI (Sacubitril/Valsartan) is the preferred RAS blocker for HFrEF, offering superior outcomes to ARBs. This patient is currently on Valsartan (ARB). While this is appropriate for the acute phase, the team should document a plan to consider upgrading to ARNI at the next clinic visit, provided BP and renal function permit."

5. OVERALL - NO PCI DONE (COROS Pending)

"Overall, this patient has not yet undergone COROS (coronary angiography) as she remains unable to lie flat due to persistent orthopnea. Once she achieves adequate decongestion and can lie supine, coronary angiography should proceed as planned - this is the key outstanding investigation that will determine whether her HFrEF is ischemic in etiology and whether revascularization (PCI or CABG) could be offered."
"The NPS viability study will help determine whether viable hibernating myocardium is present - if so, revascularization is more likely to improve LVEF and outcomes. If the myocardium is largely scarred (non-viable), medical management remains the cornerstone."

6. THANK YOU

"In summary: Madam NS is a 64-year-old lady with multiple comorbidities admitted for acute decompensated HFrEF. She was treated with a combination of IV furosemide, albumin infusion, and all four Foundational HF Medications (SGLT2i, beta-blocker, ARB, and MRA) per CPG Malaysia Heart Failure 2023 guidelines. Several PCIs were identified - most notably dose omissions for IV furosemide, an SGLT2i dose discrepancy, and the recommendation to plan for ARNI upgrade. The patient remains pending COROS for coronary anatomy assessment. Thank you for your attention."

SUPPLEMENTARY QUICK-REFERENCE: ALTERNATIVE DRUG OPTIONS

For your preceptor's questions on "what other choices are available":
Drug ClassOptions AvailableCPG Malaysia Preference
RAS BlockerACEi (Ramipril, Lisinopril, Enalapril), ARB (Valsartan, Candesartan), ARNI (Sacubitril/Valsartan)ARNI preferred if tolerated; ARB if ACEi not tolerated (cough, angioedema)
Beta-BlockerBisoprolol, Carvedilol, Metoprolol succinate (these 3 ONLY have proven HF mortality benefit)All three are Class I; Bisoprolol/metoprolol preferred in asthma/COPD
MRASpironolactone, EplerenoneSpironolactone first-line; Eplerenone preferred in males with gynecomastia
SGLT2iDapagliflozin 10mg OD, Empagliflozin 10mg ODBoth equally recommended; approved for eGFR ≥20 (Empa) and ≥30 (Dapa)
Loop DiureticFurosemide, Bumetanide, TorsemideFurosemide most common; Torsemide has better bioavailability
Additional agentsIvabradine (HR >70 in sinus rhythm), Hydralazine+ISDN (if RAS blocker not tolerated), Vericiguat (worsening HF post-hospitalization), Digoxin (persistent symptoms), Sacubitril/ValsartanSecond-line agents when foundational medications are suboptimal
Sources used: CPG Malaysia Management of Heart Failure 2023 (5th Edition) - National Heart Association Malaysia/MOH; Goldman-Cecil Medicine (International Ed.); Braunwald's Heart Disease 2 Vol Set; Goodman & Gilman's Pharmacological Basis of Therapeutics; DAPA-HF Trial; EMPEROR-Reduced Trial; RALES Trial; CIBIS-II Trial; ESC 2023 Focused Update on Heart Failure.Both scripts are complete. Here is a summary of everything prepared for you:

What Was Covered

Your Terminology Questions - Answered:

  • COROS = Coronary Angiography (CT or invasive) to visualize coronary arteries and identify ischemic cause of her HFrEF. Requires lying flat. Plan for PCI if obstructive disease found.
  • NPS (Nuclear Perfusion Study) = SPECT-based nuclear imaging to assess myocardial viability - determines if her globally hypokinetic heart has hibernating muscle that could recover after revascularization.
  • RP = Renal Profile (urea, creatinine, electrolytes, eGFR) - monitored daily in HF patients on diuretics, RAAS blockers, and MRA.
  • CA-125 = 257 = Tumor marker, elevated. BUT in this context almost certainly from HF-related serosal congestion (peritoneum, pleura) - NOT malignancy. USG abdomen confirmed no mass.
  • BP Unsupported = Patient maintaining her own BP without vasopressors/inotropic support.

PCIs (Potential Clinical Issues) Identified:

  1. IV Furosemide 80mg TDS - 4pm and 12am doses NOT given - major medication omission
  2. Empagliflozin 25mg given instead of Dapagliflozin 10mg - wrong agent AND wrong dose (HF dose is 10mg, not 25mg)
  3. Spironolactone inconsistently administered across multiple days
  4. ARNI (Sacubitril/Valsartan) not discussed for future upgrade - CPG Malaysia 2023 recommends ARNI as preferred RAS blocker in HFrEF

Two Complete Scripts Generated:

  • Script 1 (CP2 format): Problem → medication → indication → appropriateness → PCI where relevant
  • Script 2 (Storytelling format): Diagnosis narrative first, then medications woven into the story day by day
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