Nursing Field Notes / Cardio · Pathophysiology Course

MI 💔

Myocardial Infarction — the heart muscle DIES

NG-071 Cardio · ACS ADHD-friendly visual edition

Myocardial Infarction (MI) = the heart muscle DIES — “necrosis” — from lack of oxygen. This happens when there's a blockage of the coronary arteries, the “O₂ tubes” feeding the heart. The blockage is almost always a ruptured atherosclerotic plaque + clot — stage 4 of NG-145. Time = muscle.

📄 Simple Nursing original — opens in Drive →

💥 Plaque SNAP → clotAtherosclerosis stage 4. The clot — not the narrowing — is what infarcts.

📈 ST ↑ = STEMIFull-thickness, artery fully blocked → reperfuse NOW. ST ↓ / T inversion + troponin = NSTEMI.

🧪 Troponin is the answerMost specific marker. Up by 3–4 h, peaks 12–24 h, stays up 10–14 days.

⏱️ EKG in 10 minutesAny chest pain: EKG first, then labs. Aspirin chewed early.

🧨

CAUSE

STEP 1 · THE BLOCKED O₂ TUBE

The coronary arteries feed the heart itself. Block one, and the muscle downstream starves, then dies.

💔 Ischemia → Injury → Infarct: three zones, one blockage

PATHO TIP Necrosis begins within about 20–40 minutes of total occlusion and spreads outward from the inner layer (subendocardium) toward the outer layer over the next several hours. That is why every minute of door-to-balloon time is muscle.

🧠 “Ring of fire.” Dead center 🔴, burning ring 🟠, smoky edge 🟡. The EKG shows you which ring you're looking at: Q = dead · ST = injury · T = ischemia.

⚠️ Causes — “SODDA”

Letter	Risk factor	The accurate detail
S	Stress · Smoking · Stimulants	Caffeine, amphetamines, cocaine — cocaine causes coronary spasm plus clotting (see NG-098)
O	Obesity	BMI 25–29.9 = overweight · ≥30 = obesity. Central/abdominal fat carries the most risk.
D	Diabetes & hypertension	Older texts: HTN >140/90. 2017 ACC/AHA: HTN starts at ≥130/80; ≥140/90 is stage 2.
D	Diet	High cholesterol, animal & trans fats → feeds the plaque (NG-145 & NG-242)
A	Age & sex	Risk climbs for men ≥45, women ≥55. Men earlier than women; women catch up after menopause. Black adults carry a higher CVD burden — driven largely by access, chronic stress & social determinants.

🧠 “SODDA pops the artery.” Picture a shaken soda can — Stress, Obesity, Diabetes, Diet, Age. Shake it long enough and it bursts, exactly like the plaque.

📈 The progression — “CAM”

C — CAD “coronary artery disease” plaque is building

▼

A — ACS “acute coronary syndrome” the umbrella term

▼

🙂 Stable angina — “Safer” — relieved by rest & nitro

😰 Unstable angina — “Unsafe” — UNrelieved, at rest, troponin negative

▼

M — MI — heart muscle dies, troponin positive

ACS = unstable angina + NSTEMI + STEMI. The one thing that separates unstable angina from NSTEMI is the troponin.

🧠 “CAM” films the whole movie: CAD builds the set → ACS is opening night → MI is the tragedy. Stable = safer, unstable = unsafe.

💔 The MI that isn't a plaque

Most MIs are type 1 — plaque rupture + thrombus. But the muscle can also die when supply and demand split apart:

🌀 Coronary spasm — Prinzmetal/variant angina, cocaine (NG-098)
📉 Severe hypotension / shock — no pressure, no coronary flow
🫀 Sustained tachydysrhythmia — demand outruns supply
🩸 Severe anemia or hypoxia — the blood arrives, but empty-handed
💉 Coronary embolus or dissection

🧠 Supply vs demand — the heart's checkbook. An MI happens when the heart spends more O₂ than the coronary account can deliver, no matter why the account is short.

🔎

CLUES

STEP 2 · SPOT IT

Classic crushing chest pain is one presentation — and the one that kills quietly is the one that doesn't look like that.

🚨 Signs & symptoms — the classic picture

PAIN: substernal chest pain radiating to the jaw, neck, left arm, mid-back/shoulder, or felt as heartburn (epigastric).

KEY WORDS = PRIORITY “Sudden” · “Crushing” · “Radiating” — if the stem says any of these, treat it as cardiac until proven otherwise.

🫁 SOB — “dyspnea,” “labored breathing”
🤢 Nausea, vomiting, abdominal pain
💦 Diaphoresis — sweating, often cold and drenching
🥶 Pale, cool, “dusky” skin
😰 Anxiety — classic “impending sense of doom”
😵 Dizziness, syncope, palpitations

🧠 Angina takes a break; an MI does not. Rest + up to 3 nitro and the pain is still there → the muscle is dying, not just complaining.

⭐ ATYPICAL presentations — women, diabetics & older adults

NCLEX TIP A woman or diabetic with unexplained fatigue, nausea and dyspnea gets an EKG — not an antacid. Delay in recognition is a documented reason women have worse MI outcomes.

🧠 “Women whisper, men shout.” The classic elephant-on-the-chest is the loud version. In women, diabetics and older adults, the MI whispers: tired, nauseated, short of breath, jaw aches. Believe the whisper.

🆚 STEMI vs NSTEMI vs Unstable angina

	STEMI	NSTEMI	Unstable angina
Artery	100% occluded — complete, sustained	Partly / intermittently occluded	Partly occluded, no muscle death yet
Depth of damage	Transmural — full thickness of the wall	Subendocardial — inner layer only	None (ischemia only)
EKG	ST ELEVATION in ≥2 contiguous leads (new LBBB is treated as an equivalent); Q waves may develop	ST depression and/or T-wave inversion — or a normal EKG	ST depression / T inversion / normal
Troponin	✅ POSITIVE	✅ POSITIVE	❌ NEGATIVE — this is the whole difference
Treatment urgency	Immediate reperfusion — PCI target ≤90 min door-to-balloon (≤120 min if transferring); fibrinolytic ≤30 min door-to-needle if PCI unavailable	Antithrombotic therapy + risk stratification; cath usually within 24–72 h, sooner if high risk or unstable	Same anti-ischemic therapy, then stratify

Why the depth matters: a full-thickness (transmural) injury pushes the ST segment up; an inner-layer (subendocardial) injury pushes it down. Same disease, different depth, opposite arrow.

🧠 “ST UP = artery SHUT. ST DOWN = partly around.” And troponin is the tie-breaker between NSTEMI (positive) and unstable angina (negative).

📈

EKG & LABS

STEP 3 · READ THE PROOF

EKG first — within 10 minutes of arrival for any chest pain. Then serial troponins. The EKG tells you how fast; the troponin tells you whether.

📈 The four tracings you must recognize on sight

🧠 “Elevation = elimination. Depression = deprivation.” ST up means the artery is eliminated (fully shut) — go to the cath lab. ST down / T flipped means the muscle is only deprived — treat, then stratify.

🪦 Pathologic Q wave = the scar

Q waves usually appear hours to days after the infarct and are often permanent — the EKG's tattoo of an old MI.

🧠 Q = “Quit.” That muscle quit for good. ST elevation is happening now; a pathologic Q already happened.

⏱️ Order of operations

12-lead EKG within 10 min of arrival — for any chest pain or MI symptoms

Serial troponins — a baseline plus repeat draws per the assay/protocol

Continuous cardiac monitoring + IV access + O₂ if hypoxic

Echo (wall motion, EF) · CXR · cath for the definitive picture

🧠 “Strip before you stick.” EKG comes before labs — a STEMI on the strip sends her to the cath lab before a single troponin has resulted.

🧪 Cardiac markers — troponin vs CK-MB vs myoglobin

Marker	Rises	Peaks	Back to normal	Why you'd use it
Troponin I / T ⭐	3–4 h (high-sensitivity assays: 1–3 h)	12–24 h	10–14 days	The diagnostic marker. Most cardiac-specific. Serial draws show the rise and fall.
CK-MB	4–6 h	12–24 h	48–72 h	Because it clears fast, a second rise flags RE-infarction while troponin is still elevated.
Myoglobin	1–3 h — earliest	6–9 h	~24 h	Fast but not specific — rises with any muscle injury. Mostly historical now.
hs-CRP	Inflammation, not injury			Risk stratification only — not an MI diagnostic

SOURCE CHECK A single number like >0.5 ng/mL gets quoted a lot, but troponin cut-offs are assay- and lab-specific — always read the reference range printed on that lab report. And troponin is not the only marker of cardiac injury: it also rises in renal failure, heart failure, PE, sepsis, myocarditis and cardiac contusion. What confirms MI is a rise-and-fall pattern plus a clinical picture, not one number in isolation.

🧠 “Troponin is the tattoo, CK-MB is the sticker.” The tattoo stays for two weeks (great for a late arrival, useless for spotting a second MI). The sticker washes off in 2–3 days — so if CK-MB climbs again, she's re-infarcting.

🗺️

WHICH ARTERY, WHICH WALL

STEP 4 · LOCALIZE IT

The leads with ST elevation tell you which artery is blocked — and which artery tells you which complication to watch for.

🫀 The coronary tree — who feeds what

Artery	Wall it feeds	Leads with changes	Watch for
LAD left anterior descending	ANTERIOR wall + SEPTUM + much of the left ventricle	V1 V2 septal · V3 V4 anterior	The “widow-maker.” Biggest infarcts → heart failure, cardiogenic shock, ↓EF, bundle branch blocks
LCx left circumflex	LATERAL wall of the left ventricle (± posterior)	I aVL V5 V6	Often quieter on the 12-lead — posterior involvement can hide as ST depression in V1–V2
RCA right coronary	INFERIOR wall, right ventricle, and in most people the SA & AV nodes	II III aVF	Bradycardia & heart blocks · nausea/vomiting · RV infarct → preload dependent
Left main	Feeds LAD + LCx = most of the left ventricle	Widespread changes	Catastrophic — very high mortality

🧠 “I See All Leads” for the four walls: Inferior = II, III, aVF · Septal = V1–V2 · Anterior = V3–V4 · Lateral = I, aVL, V5–V6. And the artery order matches: RCA → inferior, LAD → septal + anterior, LCx → lateral.

🚨 Inferior MI: the nitro trap

Answer first: Be very cautious with nitroglycerin in an inferior (RCA) MI — up to about half of inferior MIs involve the right ventricle.

The infarcted RV can't pump forward — it survives on preload
Nitro drops preload → BP can crash suddenly and severely
Clues: inferior ST elevation + hypotension + clear lungs + JVD
Confirm with right-sided leads (V4R)
Treatment leans on IV fluids to fill the RV

🧠 “Inferior = fill her, not chill her.” A right ventricle in trouble wants volume, not vasodilation. Hypotension + clear lungs + JVD after nitro = you just emptied the RV.

💔 Complications by timeline

⚡ Minutes–hours: dysrhythmias — V-fib is the leading cause of early death after MI. This is why she's on a monitor.
🫁 Hours–days: heart failure & cardiogenic shock — crackles, ↓BP, ↓urine, cool skin (NG-196)
🔊 Days: papillary muscle rupture → sudden new murmur + flash pulmonary edema
💥 Days: ventricular free-wall or septal rupture → sudden collapse, tamponade
🩹 Days–weeks: pericarditis — sharp pain, better sitting forward, friction rub (Dressler syndrome later)
🎈 Weeks: ventricular aneurysm & mural thrombus → embolic stroke risk

🧠 “First the rhythm, then the pump, then the plumbing tears.” That's the order complications arrive — and the order you assess for them.

🩺

CARE

STEP 5 · DURING & AFTER

During the pain: MONA (with modern asterisks). After: stabilize the clot, rest the heart, and send her home able to protect it.

🚨 DURING — any chest pain: MONA, updated

MMorphine — for pain unrelieved by nitro. Qualified now: use judiciously.

OOxygen — only if SpO₂ <90% or she's in distress. Not routine anymore.

NNitroglycerin — SL 0.4 mg q5 min, max 3 doses.

AAspirin — CHEWED, non-enteric-coated, 162–325 mg. Give it FIRST.

Why morphine got an asterisk: it still relieves pain, anxiety and preload — but registry data linked morphine to worse outcomes in NSTE-ACS, and it slows absorption of oral antiplatelets (clopidogrel/ticagrelor), delaying their effect. It also masks ongoing ischemic pain, which is one of your best assessment tools. So: reasonable for continuing pain in STEMI, used cautiously and not as a reflex.

Why oxygen got an asterisk: in patients who are not hypoxic, routine O₂ showed no benefit and possible harm — hyperoxia causes coronary vasoconstriction and free-radical injury. Titrate O₂ to a target, don't hand out a nasal cannula by habit.

The real order in practice: Aspirin chewed → Nitro → O₂ only if hypoxic → Morphine only if pain persists. Nurses often say “ANOM” to remember the true sequence.

🧠 MONA still gets you the 4 drugs — but she's changed her order. Say: “Aspirin first, nitro next, oxygen only if she's blue, morphine only if she's still hurting.”

💊 Nitroglycerin — the hold rules

💊 SL 0.4 mg q5 min × 3 max. Pain still there after 3? = MI (injury) — activate EMS/the MI protocol.
📉 Nitro drip: hold/stop if SBP <90 or a drop of >30 mmHg from her baseline
💥 NEVER with a PDE-5 inhibitor — sildenafil and the other “-afil” drugs — the combination can cause fatal hypotension (avoid within 24 h; ~48 h for tadalafil)
⚠️ Caution in RV/inferior MI — preload dependent (see above)
🤕 Headache is expected — it means it's working & potent
🪑 Change positions slowly — orthostatic hypotension/syncope
🌡️ Store in the dark glass bottle, replace per expiration; sit or lie down before taking

🧠 “3 strikes and she's OUT — to the ER.” Three nitro, five minutes apart. Still hurting = infarction, not angina.

🩸 Clot stabilization — heparin

🛑 Heparin PREVENTS clot growth — it does NOT dissolve an existing clot
💥 Only fibrinolytics ("-ase": alteplase, tenecteplase) actually dissolve clot
🧪 Monitor aPTT for IV unfractionated heparin. A commonly taught therapeutic range is 46–70 seconds, but every lab publishes its own — the real target is about 1.5–2.5 × the control value
💉 Antidote: protamine sulfate
🩸 Monitor platelets — a falling platelet count on heparin suggests HIT
📋 Low-molecular-weight heparin (enoxaparin) doesn't need routine aPTT monitoring

SOURCE CHECK A “3× max” is sometimes written for aPTT; the safer teaching is above roughly 2.5× control = bleeding risk. Follow the range printed by your lab.

🧠 “Heparin holds, -ase erases.” Heparin holds the clot where it is; the “-ase” drugs erase it. Warfarin → INR/vitamin K · Heparin → aPTT/protamine.

💊 AFTER the MI — the take-home drug set

Class	Job	Nursing watch
A — Antiplatelets aspirin + clopidogrel	Stop new platelet plugs — especially critical after a stent	Bleeding, bruising, black stools. Many protocols hold if platelets fall to about 50,000/mm³ or less (normal 150–400 K) — follow the order. Antiplatelets are followed by platelet count, not INR or aPTT.
C — Cholesterol lowering “-statin”	Lower LDL and stabilize the plaque cap (NG-145 / NG-242)	Muscle pain/tenderness without injury → report; liver enzymes; no grapefruit; take in the evening
B — Beta blockers “-olol” e.g. metoprolol, atenolol	Lower HR & BP → less O₂ demand, fewer dysrhythmias, less remodeling	Hold parameters: typically HR <60 or SBP <90–100 (per order). Never stop abruptly — rebound tachycardia, HTN and angina
A — ACE inhibitors “-pril” then ARBs “-sartan”	Prevent ventricular remodeling after MI; ACE is first-line, ARB if she can't tolerate ACE	Cough & angioedema = ACE only · monitor K⁺ 3.5–5.0 mEq/L and creatinine (about 0.6–1.2 mg/dL) · avoid in pregnancy · hold for low BP (not low HR)
Nitrates isosorbide	Vasodilate — “a pillow for the heart”	Headache, orthostatic hypotension, never with “-afil”
CCBs diltiazem, verapamil, nifedipine	Vasodilate and (non-dihydropyridines) slow the heart	Diltiazem & verapamil ↓ HR and contractility. “-dipine” drugs are mainly vasodilators and can cause reflex tachycardia — don't expect them to lower the heart rate

EXAM TIP Beta blockers can mask hypoglycemia in diabetics — they blunt the tremor and tachycardia. Diaphoresis still comes through, so teach her to check glucose rather than wait to “feel low.” Also caution with asthma/COPD (bronchospasm, especially nonselective agents) and in acute decompensated heart failure.

🧠 “ABCA” — the post-MI alphabet: Antiplatelet · Beta blocker · Cholesterol statin · ACE inhibitor. Four bottles on the nightstand, four different jobs: don't clot, don't race, don't clog, don't remodel.

🏠 DISCHARGE — “DRESS” her to go home

Diet — low sodium & fluid restriction as ordered (a commonly taught target is 2 g sodium / 2 L fluid per day). Report new, rapid weight gain — that's water, and water means heart failure. Daily weights: same time, same scale, same clothes.

Reduce stress, alcohol, caffeine and cholesterol (animal fats)

Exercise — build toward about 30 min × 5 days/week, through cardiac rehab. Stop and rest for chest pain, and take nitro as prescribed.

Smoking cessation — the single highest-yield change she can make

Sex — generally safe to resume when she can climb 2 flights of stairs with no SOB or chest pain. No erectile-dysfunction “-afil” drugs with nitrates.

NCLEX TIP AVOID NSAIDs (ibuprofen, naproxen) after MI — they increase cardiovascular/clot risk and can blunt aspirin's effect.

🧠 “Get DRESSed before you leave.” Diet · Reduce · Exercise · Smoking · Sex. And the stair test is the one she'll actually remember: two flights, no huffing.

⚡ K⁺ & the monitor

🧪 Potassium 3.5–5.0 mEq/L — ACE inhibitors and ARBs push it up
🥗 Teach: avoid salt substitutes (they're potassium chloride) and don't load up on high-potassium foods without checking
📈 High K⁺ = peaked T waves, widening QRS, ST changes → cardiac monitor first
💪 Watch for muscle cramps, spasms, weakness
📉 Low K⁺ (from diuretics) is just as arrhythmogenic — flattened T, U waves

🧠 “Peaked T = potassium's peak.” Tall pointy T waves after starting a “-pril” or “-sartan” = check the K⁺ and get her on the monitor.

✅ Nursing priorities in the first hour

1️⃣ Assess — pain (OPQRST), vitals, SpO₂, lung sounds, skin
2️⃣ 12-lead EKG within 10 min + continuous monitoring
3️⃣ Aspirin chewed, IV access ×2, labs including troponin
4️⃣ Nitro per protocol with BP before/after every dose
5️⃣ Semi-Fowler's, calm environment, keep her at rest — reduce O₂ demand
6️⃣ Prepare for reperfusion — cath lab consent, NPO, check bleeding contraindications if fibrinolytics
7️⃣ Stay with her — anxiety itself raises catecholamines and O₂ demand

🧠 Everything in that list does one of two things: raise O₂ supply or lower O₂ demand. If an answer choice does neither, it isn't the priority.

⚡

QUICK RECALL

SAY IT OUT LOUD

📈 ST ↑ = STEMIFull thickness · fully blocked · reperfuse now. ST ↓ / T flip + troponin = NSTEMI.

🧪 Troponin 3–4 h → 10–14 dCK-MB clears in 48–72 h → catches re-infarction.

💊 A-N-O-MAspirin chewed · nitro ×3 · O₂ only if SpO₂ <90% · morphine only if still hurting.

🗺️ II·III·aVF = RCAInferior MI → bradycardia, blocks, RV infarct → careful with nitro.

🎯 Cover & check — 8 rapid-fire questions

Q1: What's the one lab that separates NSTEMI from unstable angina?

Troponin. Positive = NSTEMI (muscle died). Negative = unstable angina (ischemia only). Both can show ST depression or T-wave inversion.

Q2: A client with chest pain has ST elevation in II, III and aVF. Which artery, and what's your nitro concern?

RCA — inferior wall MI. Up to half involve the right ventricle, which is preload dependent, so nitroglycerin can cause severe hypotension. Look for hypotension + clear lungs + JVD, get right-sided leads (V4R), and expect fluids.

Q3: When do you give oxygen in an MI?

Only if SpO₂ is below about 90% or she's in respiratory distress. Routine oxygen in a non-hypoxic patient gives no benefit and hyperoxia can cause coronary vasoconstriction.

Q4: Chest pain, 3 SL nitro 5 minutes apart, still hurting. Interpretation?

Pain unrelieved after the 3-dose max = MI (injury), not stable angina. Activate the MI protocol / EMS — this is not "try a fourth."

Q5: Troponin has been elevated for 5 days; she gets new chest pain. Which marker helps?

CK-MB — it returns to normal in 48–72 hours, so a new rise flags RE-infarction while troponin is still elevated from the first event.

Q6: A 58-year-old woman with diabetes reports 2 weeks of fatigue, nausea and jaw ache, no chest pain. Next action?

12-lead EKG and troponin. This is the classic atypical/silent presentation — autonomic neuropathy blunts pain, and women frequently present without crushing chest pain.

Q7: Which four drug classes go home with almost every post-MI client?

Antiplatelet (aspirin ± clopidogrel), Beta blocker, Cholesterol-lowering statin, ACE inhibitor (or ARB). "ABCA": don't clot, don't race, don't clog, don't remodel.

Q8: She asks when she can have sex again.

Generally when she can climb 2 flights of stairs without shortness of breath or chest pain, per her provider. And never combine nitrates with "-afil" ED drugs.

📌

STUDY SHEETS

FROM YOUR SAVED SET

Heart attack, cardiac arrest and heart failure side by side — the one-line pearl is pump weak, artery blocked, heart stops. — swipe it sideways if it is cut off, or tap to open it full size.

Troponin and BNP — what each detects, the normal and abnormal values, and the fact that troponin rises in 2 to 4 hours and stays up 7 to 14 days. — swipe it sideways if it is cut off, or tap to open it full size.

Saved study graphics from your own collection. Each one is someone else’s work — check anything clinical against your course materials before you rely on it.