Nursing Field Notes / Cardio · Pathophysiology Course
Cardiomyopathy 🫀
Three different diseases of the heart muscle itself — dilated, hypertrophic, restrictive
NG-197CARDIOADHD-friendly visual edition
Cardiomyopathy is disease of the heart muscle itself, and it comes in three shapes: Dilated (a stretched, floppy muscle), Hypertrophic (a huge, thickened muscle that can block outflow), and Restrictive (a rock-hard, stiff muscle that can't relax). All three end the same way — LESS cardiac output, LESS oxygen-rich blood out to the body.
🏆 HypertrophicHuge trophy-like muscle can block the aorta — sudden death in young athletes.
🧱 RestrictiveRock-hard muscle can't refill — emboli are common.
🚫 NO DDD in HCMNo Dilators, Digoxin, Diuretics — they worsen the outflow block.
🧨
CAUSE
STEP 1 · THREE SHAPES, ONE PROBLEM
Same end result — less cardiac output — but the muscle gets there three completely different ways. The shape tells you everything else.
🫀 Heart-shape comparison: how each chamber geometry differs from normal
EXAM TIP All three cardiomyopathies drop cardiac output — but they get a very different-shaped heart to do it.
🧠 "Distended, Trophy, Rock-hard."Dilated = Distended thin balloon. Hypertrophic = Huge trophy-like muscle in the septum. Restrictive = Rock-hard, can't RE-fill. Say the shape, get the disease.
Fibrosis (stiff, hard scarring) of the myocardium & endocardium plus dilated chambers — a stretched, floppy muscle that struggles to squeeze oxygen-rich blood out.
The muscle — especially the septum — grows huge and thick, which can obstruct the aortic valve/outflow tract, blocking oxygenated blood from reaching the body.
Obstructive
Non-obstructive
Blocks the aortic valve outflow
Does not block outflow
🧠 Mostly genetic (autosomal dominant) — the #1 reason to screen family members of a young sudden cardiac death victim.
🧱 Restrictive cardiomyopathy — "rock-hard muscle"
The heart muscle becomes stiff and can't RE-fill during diastole — REstrictive. Emboli (blood clots) are common because blood stagnates in a chamber that won't relax and empty well.
Common causes: amyloidosis, sarcoidosis, hemochromatosis, endomyocardial fibrosis.
🧠 A rock doesn't stretch to catch water — a stiff ventricle doesn't stretch to catch returning blood.
🔎
CLUES
STEP 2 · SPOT IT
A murmur that breaks the normal rules, a lab that grades how bad the failure is, and the sign that makes hypertrophic the deadliest of the three.
🚨 Hypertrophic cardiomyopathy — sudden cardiac death in young athletes
Typically asymptomatic — no s/s — until heavy exercise, when the thickened septum obstructs outflow during high demand and the client can die suddenly. This is why HCM is the classic cause of sudden collapse in young, seemingly healthy athletes.
🧠 "Fine until the finish line." A perfectly healthy-looking teen athlete who collapses during a game is the textbook HCM story — screen family history before it happens, not after.
🔊 The murmur that breaks the rules — louder with Valsalva/standing
Most murmurs get quieter when preload drops (Valsalva strain, standing) because there's less blood to make noise. HCM is the opposite: less blood in the ventricle lets the thick septum obstruct the outflow tract more, so the murmur gets LOUDER. Squatting or lying down (more preload) makes it softer.
🧠 "HCM plays by opposite rules." If a murmur gets LOUDER with Valsalva or standing, and softer with squatting/lying flat — that's hypertrophic cardiomyopathy, not a normal flow murmur.
🧪 BNP — grades how bad the failure is
B-type (brain) natriuretic peptide is released when ventricles stretch/strain — the higher it climbs, the worse the heart failure.
🧠 Bigger number = bigger stretch. BNP is the heart shouting how hard it's straining to keep up.
📉 General signs across all three
😮💨 Low oxygen, fatigue, dizziness, syncope
😵 Restlessness, agitation, altered LOC (poor perfusion)
🫁 Left-sided failure → lung fluid (crackles)
💧 Right-sided failure → edema, ascites, JVD
🔊 New murmur (often S3), cardiomegaly
🧠 Same heart-failure playbook you already know — cardiomyopathy is just the muscle problem causing it.
🩻 Angiography — highlights coronary arteries, rules out ischemic heart disease as the cause
🧠 EF tells you the pump strength; angiography tells you why. Rule out a blocked artery before calling it a primary cardiomyopathy.
🩺
CARE
STEP 3 · PROTECT THE PUMP
Pharmacology flips for hypertrophic — know the "NO DDD" rule cold, and check three numbers before every digoxin dose.
💊 Hypertrophic cardiomyopathy pharmacology
✅ Give — reduce contractility, slow HR, let it fill
❌ NO DDD — worsens the obstruction
Beta blockers
Dilators
Calcium channel blockers
Digoxin
Diuretics
🧠 "BC, no DDD." Beta blockers & Calcium channel blockers slow the heart and give it more time to fill around the obstruction. Dilators, Digoxin, and Diuretics all shrink ventricular volume or boost contractility — both make the outflow obstruction worse.
🏆 HypertrophicSudden death in young athletes; murmur LOUDER with Valsalva/standing
🧱 RestrictiveRock-hard, can't refill, emboli common
🚫 NO DDD in HCMNo Dilators, Digoxin, Diuretics — check pulse/K+/level before any dose
🎯 Cover & check — 4 rapid-fire questions
Q1: Which cardiomyopathy is the classic cause of sudden cardiac death in young athletes, and why?
Hypertrophic cardiomyopathy — the thickened septum can obstruct the aortic outflow tract, especially during heavy exertion, causing sudden collapse in someone who was often asymptomatic.
Q2: What happens to the HCM murmur with Valsalva or standing, and why is that the opposite of most murmurs?
It gets LOUDER. Less ventricular volume lets the thick septum obstruct the outflow tract more. Most other murmurs get softer with less blood volume.
Q3: What three numbers must be checked before giving digoxin?
Apical pulse (hold if <60), potassium (hold/notify if <3.5, raises toxicity risk), and digoxin level (hold if >2.0, toxic).
Q4: What does "NO DDD" mean for hypertrophic cardiomyopathy?
Avoid Dilators, Digoxin, and Diuretics — they reduce ventricular volume or increase contractility, both of which worsen the outflow obstruction.