ACS, STEMI Management, Post-PCI Nursing & Heart Failure for GCC CCU Nurses
CCU / Acute Coronary Syndrome
ACS Classification & Diagnosis
The ACS Spectrum
Condition
Troponin
ECG Changes
ST Elevation
Unstable Angina (UA)
Normal
Possible ST depression / T-wave inversion
No
NSTEMI
Elevated
ST depression, T-wave inversion, or normal
No
STEMI
Elevated
ST elevation ≥1mm limb leads; ≥2mm precordial
Yes (or new LBBB)
Key Clinical Point: UA and NSTEMI are distinguished only by troponin result — both present without ST elevation. Troponin should be measured at 0h and 3h (high-sensitivity assay) or 0h and 6h (conventional).
STEMI Diagnostic Criteria
Voltage Criteria
Limb leads (I, II, III, aVL, aVF): ≥1 mm ST elevation in ≥2 contiguous leads
Precordial leads (V1–V6): ≥2 mm ST elevation in ≥2 contiguous leads
New LBBB with typical ischaemic symptoms — treat as STEMI-equivalent
What Counts as Contiguous?
V1, V2, V3, V4 are contiguous (precordial)
II, III, aVF are contiguous (inferior)
I, aVL, V5, V6 are contiguous (lateral)
Lead pairs must share anatomical territory
STEMI Territory & Culprit Artery
Territory
Leads with ST Elevation
Culprit Artery
Special Considerations
Anterior
V1 – V4
LAD
Largest territory — worst prognosis; watch for cardiogenic shock
Inferior
II, III, aVF
RCA (80%)
Check V4R for RV infarct; watch for bradycardia, heart block
Lateral
I, aVL, V5, V6
LCx
Often overlooked; reciprocal changes in inferior leads
Posterior
Reciprocal ST ↓ V1–V2; dominant R in V1
RCA / LCx
Do posterior leads (V7–V9); ST elevation in posterior leads confirms
RV Infarct
ST elevation in V4R
RCA (proximal)
Fluid-sensitive! Avoid nitrates & diuretics — give IV fluids
RV Infarct Alert: Inferior STEMI + hypotension = suspect RV infarct. Obtain right-sided leads (V3R, V4R). ST elevation >1mm in V4R is diagnostic. Treatment: IV fluid bolus 250mL NS — do NOT give nitrates.
Intermediate 109–140: 1–3% → consider early invasive
High risk >140: >3% → early invasive within 24h
TIMI Score (NSTEMI/UA)
7-item score (0–7): age ≥65, ≥3 CAD risk factors, prior stenosis ≥50%, ST deviation, ≥2 anginal events in 24h, aspirin use in last 7 days, elevated troponin. Score ≥3 = high risk.
Rise & fall pattern distinguishes Type 1 MI (plaque rupture) from Type 2 MI (supply-demand mismatch)
Other causes of troponin rise: PE, myocarditis, sepsis, renal failure, heart failure, cardioversion — always correlate clinically
In GCC: diabetes is highly prevalent — atypical presentations (silent MI, dyspnoea without chest pain) are common
Initial Management — MONAB Protocol
STEMI Time Target: 12-lead ECG within 10 minutes of arrival. Door-to-balloon time <90 minutes. Every minute of delay = myocardium lost. Activate the cath lab early.
MONAB — First 30 Minutes
M
Morphine — 2–5 mg IV titrated for pain relief Controversial: delays P2Y12 inhibitor absorption (especially clopidogrel); use cautiously, only if pain uncontrolled by nitrates. Consider IV fentanyl as alternative.
O
Oxygen — ONLY if SpO₂ <94% Do NOT give oxygen if SpO₂ ≥94% — hyperoxia causes coronary vasoconstriction and worsens infarct size. Evidence: AVOID-2 trial.
N
Nitrates — GTN 400 mcg sublingual (×3 every 5 min), then IV infusion Absolute contraindications: SBP <90 mmHg, RV infarct, recent PDE5 inhibitor use (sildenafil/tadalafil within 24–48h). Reduces preload and coronary spasm.
A
Aspirin — 300 mg loading dose STAT (chewed for rapid absorption), then 75 mg daily lifelong Irreversible COX-1 inhibitor — inhibits thromboxane A2-mediated platelet aggregation. Give even if patient has taken aspirin previously.
B
Beta-blocker — Metoprolol 5 mg IV (or oral Bisoprolol 2.5–5 mg if haemodynamically stable) Reduces infarct size, arrhythmias, mortality. Contraindications: cardiogenic shock, severe bradycardia (<60 bpm), AV block, severe bronchospasm, decompensated HF.
STEMI — Additional Immediate Actions
Antiplatelet Loading
Ticagrelor 180 mg loading (preferred — faster onset, more potent)
Or Clopidogrel 600 mg if ticagrelor not available / contraindicated
Prasugrel 60 mg (alternative — avoid if prior stroke/TIA, age >75, weight <60 kg)
Give P2Y12 inhibitor as early as possible (not after morphine if possible)
Anticoagulation
UFH 5,000 units IV bolus (+ infusion if not proceeding to immediate PCI)
Or Fondaparinux 2.5 mg SC (NSTEMI preferred; avoid in GFR <20)
Bivalirudin: alternative to UFH during primary PCI
Immediate Cath Lab Activation
Primary PCI is the preferred reperfusion strategy
Target: door-to-balloon <90 min
If PCI not available within 120 min: consider thrombolysis (tPA / streptokinase) + transfer
Activate cath lab team, notify interventional cardiologist, prepare patient for transfer
Pseudoaneurysm: pulsatile lump, bruit on auscultation — USS Doppler confirms; ultrasound-guided compression or thrombin injection
AV fistula: continuous bruit — USS confirms; may need surgical repair
Femoral nerve injury: weakness/paraesthesia in thigh/quadriceps
Any expanding haematoma, new bruit, or falling BP in a post-femoral PCI patient requires immediate medical review.
Post-PCI Observations — Standard Protocol
Parameter
Frequency
Target / Action
BP & HR
Every 15 min × 1h, then hourly × 4h
SBP >90, HR 60–100
12-lead ECG
Immediately post-PCI, at 24h
Compare with pre-PCI; new changes = urgent review
Continuous ECG monitoring
Minimum 24h post-STEMI
Watch for reperfusion arrhythmias (VF, AF, RBBB)
Access site
Every 30 min × 2h, then hourly
Haematoma, bleeding, distal perfusion
Pain score (NRS 0–10)
Hourly
Target ≤3; escalate if chest pain recurs
Urine output
Hourly
Target ≥0.5 mL/kg/hr; CI: contrast nephropathy
Creatinine
At 24h and 48h post-PCI
Contrast-induced nephropathy peak at 48–72h
Fluid balance
Every shift
Pre-hydrate with IV NS to protect kidneys
Contrast Nephropathy Prevention: IV normal saline 250–500 mL/h during and after PCI (if no HF). N-acetylcysteine evidence is weak. Avoid NSAIDs post-procedure. Monitor creatinine at 48h.
Post-STEMI / Post-PCI Medications
Drug Class
Drug / Dose
Duration
Key Nursing Points
Aspirin
75 mg OD
Lifelong
Never stop — stent thrombosis risk; give with food
P2Y12 Inhibitor (DAPT)
Ticagrelor 90 mg BD
Min 12 months
Do not miss doses; counsel on dyspnoea SE; no abrupt stop
Statin
Atorvastatin 40–80 mg nocte
Lifelong
Evening dose preferred; monitor for myalgia; check CK if muscle pain
Do NOT stop abruptly; titrate up slowly; monitor HR and BP
Aldosterone antagonist
Eplerenone 25–50 mg OD
Lifelong if EF ≤35% + HF or diabetes
Monitor K⁺ closely; avoid if creatinine >220 or K >5.0
DAPT Alert: Stopping dual antiplatelet therapy prematurely (especially in the first month post-DES stent) carries very high risk of stent thrombosis — a catastrophic event with ~40% mortality. Nurses must reinforce adherence at every contact.
Diagnostic Triad: SBP <90 mmHg for >30 min (or vasopressor-dependent) + Evidence of low cardiac output (oliguria, cold/clammy extremities, altered consciousness) + Elevated PCWP (>18 mmHg) — excluding other causes of hypotension
Haemodynamic Targets
MAP >65 mmHg
Urine output ≥0.5 mL/kg/hr
Lactate normalisation (<2 mmol/L)
Avoid excessive fluid — PCWP usually already elevated
Vasopressors & Inotropes
Noradrenaline (norepinephrine): first-line vasopressor — increases SVR and MAP
Dobutamine: inotrope — increases cardiac output (add to noradrenaline if CO low)
Adrenaline: second-line, increases both HR and BP but increases myocardial O₂ demand
Vasopressin: adjunct to reduce noradrenaline dose
Avoid dopamine — higher arrhythmia rate vs noradrenaline (SOAP-II trial)
Mechanical Circulatory Support
IABP (Intra-Aortic Balloon Pump):
Counterpulsation: inflates in diastole → increases coronary perfusion; deflates in systole → reduces afterload
Timing with ECG (R-wave) or arterial waveform
Nursing: check limb perfusion hourly, anticoagulation with UFH, position (30° max head elevation), balloon gas (helium)
Note: IABP-SHOCK II trial showed no mortality benefit in routine cardiogenic shock — use selectively
Impella (Axial Flow VAD):
Increasingly used in GCC centres for refractory cardiogenic shock
Placed across aortic valve — pumps blood from LV to aorta
Requires anticoagulation; monitor for haemolysis (pink urine)
Acute Pulmonary Oedema — LMNOP Protocol
L
Loop Diuretic — Frusemide (Furosemide) 40–80 mg IV stat Immediate venodilation (within 5 min) then diuresis (within 30 min). Repeat if inadequate response. Target diuresis 0.5–1 mL/kg/hr.
M
Morphine — 2–4 mg IV Reduces anxiety, causes venodilation → preload reduction. Use cautiously; can cause respiratory depression. Have naloxone available.
N
Nitrates — IV GTN infusion (start 10–20 mcg/min, titrate) Potent venodilator → preload reduction. Also reduces afterload at higher doses. Monitor BP closely; avoid if SBP <90 mmHg.
O
Oxygen — High-flow via non-rebreather mask (target SpO₂ 94–98%) Consider NIV/CPAP early if SpO₂ remains <90% or work of breathing is high. NIV reduces need for intubation by ~50%.
P
Position — Sit upright (90°), legs dependent Gravity-dependent pooling of blood in lower limbs → reduces venous return → reduces preload. Never lay flat — worsens dyspnoea.
CPAP / NIV in Cardiogenic Pulmonary Oedema
CPAP 5–10 cmH₂O: improves oxygenation, reduces work of breathing, decreases preload
BiPAP: adds inspiratory pressure support — useful if hypercapnic
Evidence (3CPO trial): NIV reduces intubation rate, improves dyspnoea, SpO₂ — no mortality difference vs pharmacotherapy alone
NEVER miss a dose — especially in first 30 days post-stent (bare metal or DES)
Ticagrelor: warn about common side effects — dyspnoea (not bronchospasm), minor bleeding
If surgical procedure needed: discuss with cardiologist; do not stop without guidance
Statin (Atorvastatin)
Evening dose preferred — hepatic cholesterol synthesis peaks overnight
Educate: statins do NOT cause liver damage at standard doses (LFTs not needed routinely)
Myalgia: common; measure CK if significant. Stop if CK >5× ULN or rhabdomyolysis suspected
ACEi / ARB
Dry cough: class effect of ACEi (bradykinin-mediated) — switch to ARB (candesartan/valsartan)
Monitor creatinine and potassium at 1–2 weeks after starting/increasing dose
Hold if dehydrated, diarrhoea/vomiting, or pre-procedure with contrast
Beta-Blocker
NEVER stop abruptly — rebound hypertension, tachycardia, angina, may precipitate MI
If patient cannot tolerate oral, discuss with team before withholding
Monitor for symptomatic bradycardia (<50 bpm) and hypotension (SBP <90)
GCC-Specific Context
Epidemiology: GCC has one of the world's highest ACS rates. Patients are often younger (40s–50s), with high prevalence of diabetes, smoking, and hypertension.
Diabetes prevalence: UAE, Saudi Arabia, Qatar — among highest globally. Atypical MI presentations (silent MI, jaw/arm pain only) are common in diabetic neuropathy.
Ramadan & cardiac medications: Patients must NOT stop medications during Ramadan. Counsel on timing adjustment — e.g., take morning medications at Suhoor (pre-dawn meal), evening doses at Iftar. Dehydration risk increases; monitor fluid balance.
Cath lab availability: Major GCC hospitals (Dubai, Abu Dhabi, Riyadh, Doha, Kuwait City) have 24/7 primary PCI capability. Know your local activation protocol and door-to-balloon targets.
Language/literacy: Provide medication instructions in Arabic when needed; use pictograms for low-literacy patients.
GRACE Score Calculator (Simplified)
Enter patient values to estimate in-hospital mortality risk for NSTEMI/UA. This is a simplified estimator — use validated tool for clinical decisions.