The whole Exam 4 block condensed — hypertension, hypotension, atherosclerosis and lipid disorders, valvular heart disease, coronary artery disease and heart failure: classification and causes, the orthostatic heart-rate tell, the lipid memory aid and 2018 statin decisions, the murmur words and valve-by-valve essentials, the troponin numbers and lead-to-artery chart, and the 2022 heart failure groups, stages and therapy.
| Term | What you need to know |
|---|---|
| Treatment goal | Below 130/80, with values closer to 120/80 encouraged where appropriate. The same number defines the condition and measures control. |
| Primary (essential) | No single identifiable underlying cause. The vast majority of adult cases. |
| Secondary | An identifiable underlying condition drives the pressure. Go looking when the pattern is wrong (see next topic). |
| Resistant | Above goal despite three complementary drugs at maximally tolerated doses. |
| Hypertensive emergency | Severe elevation with acute hypertension-mediated organ injury. No numeric cutoff exists — 230/130 with no acute organ involvement is severe asymptomatic hypertension. Qualifying injury: encephalopathy, acute pulmonary edema, acute kidney injury, aortic dissection, acute coronary syndrome. |
| White coat vs masked | White coat = high office, normal out-of-office. Masked = normal office, high out-of-office — and it carries real cardiovascular risk, which is why out-of-office measurement is not only about avoiding overtreatment. |
| Epidemiology | Roughly one in five of those affected are controlled to goal nationally. Prevalence rises sharply with age: 23.4% at 18–39 years, 52.5% at 40–59 and 71.6% at 60 and over. |
| Risk factors (primary) | Advancing age · family history · excess adiposity · high dietary sodium · inactivity · excess alcohol · dyslipidemia · insulin resistance. Low potassium intake and poor sleep are modifiable too. |
| Term | What you need to know |
|---|---|
| When to go looking | Early onset · abrupt new onset · resistance · sudden loss of previously stable control. The pattern is the clue, not any single reading. |
| Chronic kidney disease | Impaired sodium excretion expands extracellular volume, with renin-angiotensin-aldosterone and sympathetic activation. Needs an abnormality persisting ≥ 3 months. Relationship is bidirectional — evaluate diabetes rather than assuming which came first. |
| Renovascular disease | Atherosclerotic (older, vascular, often bilateral and progressive) or fibromuscular dysplasia (young). Clues: resistant or abrupt elevation · abdominal bruit · asymmetric kidneys · recurrent flash pulmonary edema · marked creatinine rise after starting an ACE inhibitor. Refer early for flash edema, progressive renal decline despite optimal therapy, or truly refractory control. |
| Primary aldosteronism | Autonomous aldosterone production independent of renin. Screen for resistant pressure, unexplained hypokalemia, adrenal incidentaloma, early or familial hypertension. Test: morning aldosterone to renin ratio, positive above roughly 20:1 with an adequate aldosterone concentration. |
| Obstructive sleep apnea | Recurrent airway obstruction → intermittent hypoxemia and arousal → sustained sympathetic activation. Snoring, witnessed apneas, daytime sleepiness. Confirm with polysomnography or validated home testing. |
| Drugs & substances | Ask beyond the prescription list: over-the-counter drugs, recreational substances, licorice, herbal supplements. Excess alcohol raises pressure chronically, and withdrawal can raise it acutely. |
| Thyroid | Hyper → raises cardiac output → systolic elevation. Hypo → raises vascular resistance → diastolic elevation. |
| Cushing syndrome | Glucocorticoid excess. Proximal muscle weakness · easy bruising · thin skin · broad purple striae · central adiposity. Test: low-dose dexamethasone suppression. |
| Pheochromocytoma | Catecholamine excess. The five Ps: pressure, perspiration, palpitations, pallor, tremor — paroxysmal, with well intervals. Test: plasma free metanephrines or 24-hour urinary fractionated metanephrines. Surgery: ALPHA blockade first, then beta — isolated beta blockade is dangerous. |
| Coarctation | Radial-femoral delay; leg systolic lower than arm (normally it is higher). Echocardiography establishes it; refer to a vascular surgeon or structural cardiologist. |
| Term | What you need to know |
|---|---|
| Heart | Left ventricular hypertrophy with impaired diastolic relaxation — independently raises risk. Progresses to heart failure with either preserved OR reduced ejection fraction, so a normal ejection fraction does not reassure. |
| Brain | Both ischemic stroke and intracerebral hemorrhage, plus small-vessel white matter change, lacunar infarcts and cognitive decline. Acute stroke follows a distinct protocol — never apply chronic targets acutely. |
| Kidney | Injury to vessels, glomeruli and interstitium. Earliest markers: rising urine albumin-to-creatinine ratio, falling estimated filtration rate — both read as trends. |
| Aorta | Dissection: abrupt severe chest/back/abdominal pain, maximal at onset, often tearing. Pulse deficits, asymmetric arm pressures, aortic regurgitation murmur, new neurological deficit. Neither normal pulses NOR a normal chest radiograph excludes it. Immediate cross-sectional vascular imaging; urgent surgery. |
| Arteries | Shear stress → intimal injury → low-density lipoprotein oxidation → smooth muscle proliferation. Treat total cardiovascular risk, not pressure alone. |
| Retina | Predicts long-term stroke risk independently of the pressure level; retinal arterial narrowing predicts future hypertension; control can produce regression. Focal narrowing, hemorrhages and exudates = current pressure. Generalized narrowing and AV nicking = current AND previous. Disc edema = emergency. |
| Term | What you need to know |
|---|---|
| Symptoms | Most patients with mild to moderate primary hypertension have no reliable blood pressure-related symptoms. Headache is common but nonspecific and cannot guide anything. |
| Immediate evaluation | Confusion or seizures · visual disturbance or focal deficit · abrupt severe headache · chest or severe back pain · oliguria. |
| Measurement technique | Rest ≥ 5 minutes, empty bladder, no smoking/caffeine/vigorous activity for 30 minutes. Back supported, feet flat, legs uncrossed, bare arm at heart level, not speaking. Cuff matched to arm circumference. At least two readings. Both arms initially — use the higher consistent arm at follow-up. |
| Why technique matters | Measurement error is one of the first things to exclude before labeling a patient resistant — bad technique mimics true resistance exactly. |
| Baseline panel | Creatinine with filtration rate, urine albumin-to-creatinine ratio, electrolytes, glucose or glycated hemoglobin, lipids, thyroid-stimulating hormone, full blood count, urinalysis. Three jobs at once: screen secondary causes, measure organ damage, set a baseline before drugs that move potassium and creatinine. |
| Electrocardiogram | Voltage criteria for hypertrophy are specific but NOT sensitive — a normal tracing does not exclude hypertensive heart disease. |
| Not routine | Chest radiograph — only for suspected pulmonary edema, cardiomegaly, or widened mediastinum. Echocardiography — only for suspected heart failure, significant murmur, hypertrophy on ECG, or unexplained dyspnea. |
| Home monitoring | Validated upper-arm device. Two readings a minute apart, morning and evening, seven days; report the average. Educate: do not overreact to the highest single reading. |
| Term | What you need to know |
|---|---|
| Lifestyle | Recommended at every blood pressure category, and continues alongside drugs. DASH-style with reduced sodium · ~150 min/week moderate aerobic plus resistance training · sustained 5–10 kg loss meaningfully lowers systolic · alcohol to low-risk thresholds (never start alcohol for cardiovascular benefit). |
| First-line classes | Thiazide-type diuretic (chlorthalidone preferred) · ACE inhibitor OR angiotensin receptor blocker · dihydropyridine calcium channel blocker. Beta blockers are deliberately absent. |
| Thiazide | Monitor electrolytes, uric acid, volume status. Hyponatremia · hypokalemia · hyperuricemia may precipitate gout · volume depletion. At 65+, check sodium — especially women and low-normal sodium. With a beta blocker: higher new-onset diabetes risk. |
| ACE inhibitor / ARB | Dry cough (bradykinin-mediated, up to ~1 in 5 → switch to an ARB) · hyperkalemia · creatinine rise · angioedema, 2–4× more common in Black patients. Avoid: pregnancy, prior angioedema, bilateral renal artery stenosis. |
| Dihydropyridine | Dependent ankle edema is commonest — vasodilatory, so a diuretic does not fix it. Also flushing, headache, gingival enlargement. |
| NEVER combine | ACE inhibitor + ARB — hyperkalemia and acute kidney injury risk with no added benefit; one is used INSTEAD of the other. Beta blocker + verapamil/diltiazem — both slow the sinus and AV nodes → severe bradycardia and heart block. Non-dihydropyridines are also avoided where the ejection fraction is reduced. |
| Beta blockers | NOT first-line for uncomplicated hypertension. Preferred where the comorbidity selects them: heart failure with reduced ejection fraction, recent myocardial infarction, ischemic disease. |
| Starting | Stage 1 → one first-line agent. Stage 2 → two complementary agents, ideally a single-pill combination (adherence is itself a main determinant of control). Preferred pairings: a renin-angiotensin blocker with either a dihydropyridine or a thiazide-type diuretic. |
| Term | What you need to know |
|---|---|
| Exclude the impostors first | Nonadherence is the commonest cause of apparent resistance. Then measurement error · white coat effect · high sodium or alcohol · interfering drugs · undiagnosed sleep apnea or secondary hypertension. |
| Step 1 | Optimize the diuretic — chlorthalidone preferred, class matched to renal function. An inadequate diuretic is a common reason the other two agents appear to fail. |
| Step 2 | Titrate the renin-angiotensin blocker and the dihydropyridine to maximally tolerated doses. |
| Step 3 | Add spironolactone — the most evidence-supported fourth agent — if filtration rate and potassium allow. |
| Step 4 | Escalate by physiology and comorbidity: beta blockade · hydralazine (reflex tachycardia and fluid retention → needs combination therapy) · clonidine (sedation, dry mouth, rebound hypertension on abrupt withdrawal). Then refer to a hypertension specialist. |
| Emergency: how fast | Reduce mean arterial pressure by no more than ~20–25% in the first hour, then toward ~160/100–110 over 2–6 hours, normalizing gradually over a day or two. |
| Emergency: why not faster | Autoregulation has adapted to the higher pressure. The organs reset the range over which they protect their own perfusion, so normalizing too fast leaves them underperfused at a value that would be safe in anyone else — causing ischemic stroke, myocardial injury or renal failure. |
| Exceptions | Aortic dissection and some stroke syndromes — acute stroke follows its own protocol. |
| Term | What you need to know |
|---|---|
| Hypotension | A decrease in systemic pressure below normal. Not a diagnosis — syncope is the result of symptomatic hypotension; treat the real diagnosis. Norms change with age; consider comorbidities and relative hypotension; each reading is a snapshot. |
| Syncope vs near-syncope | Syncope = transient, self-limited loss of consciousness and postural tone, spontaneous recovery. Near-syncope = dizziness, lightheadedness, tunnel vision without losing consciousness. |
| Acute vs chronic | Acute: sudden, usually symptomatic, specific trigger (toxic or overdose; infection = long-lasting acute). Chronic: waxes and wanes, intermittently symptomatic, cause may be unavoidable (reduced ejection fraction heart failure, cardiomyopathy). |
| Three syncope groups | Orthostatic (neurogenic, non-neurogenic) · reflex (situational, vasovagal) · cardiogenic (arrhythmia, structural, vascular). |
| Non-hypotensive syncope | Hypoglycemia, seizure, toxic overdose, electrolyte imbalance, hypoxia, anxiety, anemia, postural tachycardia syndrome. Against seizure: no tongue biting, incontinence or prolonged confusion. |
| Term | What you need to know |
|---|---|
| ★ Orthostatic criteria | Supine then standing. Systolic fall >20 or diastolic >10 mmHg within 3 minutes; systolic >30 with elevated baseline or supine hypertension. One criterion is enough (spoken). History is THE most important part. |
| ★ The big tell: heart rate | Pressure falls in both. Significant heart rate rise = non-neurogenic (intact reflex; e.g. 68 → 92). Minimal rise = neurogenic (autonomic failure; e.g. 72 → 76). |
| Neurogenic | Autonomic failure: diabetes, Parkinson disease, multiple system atrophy. Volume depletion usually absent; autonomic symptoms often present. Clue: numb feet in long-standing diabetes. |
| Non-neurogenic | Hypovolemia, medication, advanced age: diarrhea, hemorrhage, diuretics. Volume depletion often present (dry mucous membranes); autonomic symptoms usually absent. |
| Orthostatic treatment | Slow positional changes; treat the underlying cause; iatrogenic → reduce or remove the drug. |
| Vasovagal | “The common faint”, most common type, young women. Triggers: emotional stress, fear, pain, heat, prolonged standing. Warm, nauseated, sweaty prodrome. |
| Situational | A bodily function or action: cough, sneeze, micturition (voiding standing at night; alcohol, dehydration, alpha-1 blocker with lisinopril). |
| ★ Reflex diagnosis & care | History, history, history + a log of pattern and frequency. Trigger avoidance; safety precautions during unavoidable triggers. |
| Term | What you need to know |
|---|---|
| Postural orthostatic tachycardia syndrome | Heart rate rise >30 or above 120 within 10 minutes (adolescents: 40); improves lying down. Ages 15–50, women > men, Ehlers-Danlos. Tilt-table: sensitivity 40% (negative tells little), specificity >80%. Water + salt; fludrocortisone. (Deck: “positional”.) |
| Cardiogenic | Abrupt collapse without warning, palpitations, heart disease. Arrhythmia → electrocardiogram, monitor, stress test. Structural → echocardiogram, stress echo. Vascular → emergent testing in the emergency department. All: cardiology consultation. |
| ★ Drug ↔ condition | Midodrine: best with neurogenic; avoid with supine hypertension, severe heart disease, chronic kidney disease. Fludrocortisone: best with postural tachycardia syndrome; avoid in heart failure (salt and water retention). Droxidopa: mild, better with supine hypertension, adjunct. |
| Pressors | Epinephrine, norepinephrine, dopamine, phenylephrine, vasopressin: emergency department and intensive care only. |
| ★ Education | “Understanding is the key to compliance.” No dosing or mechanism questions. |
| Term | What you need to know |
|---|---|
| Memory aid: the garbage system | A story, not a fact. HDL (high-density lipoprotein) = garbage trucks (apo A-I, never apo B): excess cholesterol back to the liver and bile. LDL (low-density lipoprotein) = building-material trucks (B-100), the highest risk — clear them first; a fuel-tanker drug (fibrate) waits for triglyceride ≥500 under the 2018 guideline (he taught >200). Chylomicrons = gut fuel barges (B-48); VLDL (very-low-density) = liver fuel tankers (B-100) → IDL (intermediate-density) after drop-off. Lp(a) = delivery truck with an armored trailer. LDL receptor = the liver’s gate (broken in familial hypercholesterolemia); PCSK9 = the demolition crew. Apo E = tow ticket for empty tankers. |
| Lipoproteins | Chylomicrons: least dense, after fatty food, triglyceride. VLDL: mainly triglyceride. LDL: mostly cholesterol, “bad”, highest risk, primary target. HDL: densest, reverse cholesterol transport, “good”, raised by exercise. Lp(a): LDL-like + apo(a), causal independent risk → aggressive LDL lowering. |
| Apolipoproteins | B-48 intestine (chylomicrons) · B-100 liver (VLDL, IDL, LDL, Lp(a)) · B absent from HDL · A-I on all HDL · E critical in triglyceride clearance (E2 homozygosity → dysbetalipoproteinemia). |
| Lab bands (mg/dL) | Total <200 desirable, >240 high · LDL <100 optimal, 160–189 high, >190 very high · HDL <40 low, >60 high · Triglyceride <150 normal, 200–499 high, >500 very high. |
| Exam findings | Eruptive xanthomas (small yellow-white papules, back, buttocks, extensors) → very high triglyceride. Tendon xanthomas (Achilles, hands) → high LDL / familial hypercholesterolemia. Xanthelasma; corneal arcus before 40 → genetic. |
| Term | What you need to know |
|---|---|
| ★ Familial chylomicronemia | Fasting triglyceride >500, usually >1000; acute pancreatitis (severe abdominal pain), eruptive xanthomas, lipemia retinalis (opalescent retinal vessels). “One that can save somebody’s life.” |
| Severe hypertriglyceridemia | Triglyceride >500, high total, low HDL, usually no LDL rise; risk = pancreatitis. Very low-fat diet (<15%), weight, activity, fibrate (slide adds niacin; 2018 does not). Take an alcohol history. |
| ★ Homozygous familial hypercholesterolemia | Two mutant LDL-receptor alleles; 1 in 1 million; child with xanthomas, total ~400 to >1000, atherosclerosis before puberty. Skin biopsy (receptor activity) confirms. LDL apheresis = treatment of choice; add drugs; refractory → PCSK9 inhibitor. |
| ★ Heterozygous familial hypercholesterolemia | One allele; 1 in 250; adult with LDL 200–400, normal triglyceride, Achilles xanthomas (~75%), arcus, premature coronary disease in the family. No definitive test. High-intensity statin → ezetimibe → PCSK9 inhibitor if refractory (“don’t jump straight to the PCSK9”). |
| Other genetic types | Familial defective apo B-100: familial-hypercholesterolemia picture, 1 in 1,500. Mixed: triglyceride >150 + LDL >130 (most common in practice). Dysbetalipoproteinemia: triglyceride and total both 250–500, palmar and tuberoeruptive xanthomas, apo E2. |
| Low HDL | <40 (women <50 for metabolic syndrome). Lifestyle first: stop smoking (+10%), weight loss, aerobic exercise (+5%), healthier fats. Rule out diabetes, smoking, obesity; anabolic steroids lower it. |
| Metabolic syndrome | Any 3: waist >40 in men / >35 in women; triglyceride >150; HDL <40 men / <50 women; blood pressure >130/>85; fasting glucose >110. Lifestyle first. |
| Secondary causes | Before a statin rule out: LDL → hypothyroidism, nephrotic syndrome, primary biliary cirrhosis, anorexia. Triglyceride ≥500 → diabetes, chronic kidney disease, alcoholism, pregnancy, hypothyroidism. Low HDL → diabetes, smoking, obesity. |
| Screening | All adults ≥20. Children once at 9–11 (non-fasting), again in late adolescence; from 2 with a family history. 2018: a non-fasting full panel is fine for screening; fast only if triglyceride ≥400 (slide: triglyceride and calculated LDL need 9–12 hours). |
| Term | What you need to know |
|---|---|
| ★ LDL first, then triglyceride | “Address the LDLs, then address the triglycerides.” 2018 guideline: triglyceride 175–499 → lifestyle, secondary causes, intensify the statin; fibrate only at ≥500 (pancreatitis). He taught “>200 after the LDL goal → fibrate or niacin” (older ATP III rule). Non-HDL = total − HDL. |
| ★ Drug ↔ lipid | Statin → LDL (↓25–63%; monitor lipids, liver function, creatine kinase). Fibrate → triglyceride. Niacin → raises HDL best. Ezetimibe, bile acid sequestrant → add-on LDL. PCSK9 inhibitor (evolocumab, alirocumab) → refractory familial hypercholesterolemia / very high risk after statin + ezetimibe. Generic names only. |
| Statin intensity | By LDL fall, never milligrams: high ≥50%, moderate 30–49%, low <30%. |
| ★ 2018 risk categories | 10-year risk <5% low (lifestyle) · 5–7.5% borderline (moderate statin if enhancers) · 7.5–20% intermediate (moderate, ↓30–49%) · ≥20% high (↓≥50%). Age 40–75, LDL 70–189, no diabetes. |
| ★ 2018 statin groups | Clinical ASCVD (atherosclerotic cardiovascular disease) ≤75 → high intensity. LDL ≥190 → high intensity, no risk calculation. Diabetes 40–75 → moderate. Very high risk, LDL ≥70 on max statin → add ezetimibe, then PCSK9 inhibitor. Uncertain → coronary artery calcium (0 may defer; ≥100 statin). |
| Lifestyle | Saturated fat <7% (the course figure; his spoken 10% is the looser Dietary Guidelines limit), soluble fiber 20–30 g, plant stanols, lose 5–10%, 30 minutes activity, stop smoking. 2026 / PREVENT: rotations only, not tested. |
| Term | What you need to know |
|---|---|
| ★ The words | Harsh / rumble = stenosis → abnormal forward flow → pressure overload. Blowing = regurgitation → abnormal backflow → volume overload. No audio on the test — murmurs come as words. |
| ★ Timing | Systolic: aortic stenosis, mitral regurgitation, pulmonic stenosis, tricuspid regurgitation. Diastolic: aortic regurgitation, mitral stenosis, pulmonic regurgitation, tricuspid stenosis — “ARMS rest because they are PRetty TiredS”. |
| ★ Where (A-P-E-T-M) | Aortic 2nd right intercostal space, sternal border · Pulmonic 2nd left · Erb’s point 3rd left · Tricuspid 5th, lower left sternal border · Mitral apex, 5th space, midclavicular line. Stems give the location, not the valve name. |
| Respiration (RILE) | Right-sided louder on inspiration (more venous return) · left-sided louder on expiration. Carvallo sign = the inspiratory increase; it tells tricuspid from mitral regurgitation. |
| Heart sounds | S1 = mitral + tricuspid closing · S2 = aortic + pulmonic closing · S3 = dilated, volume-loaded ventricle (systolic failure) · S4 = hypertrophied, pressure-loaded ventricle (diastolic failure, e.g. aortic stenosis). |
| Equal weight | “Just as likely a tricuspid valve question as an aortic valve question.” Grading is tested only for aortic and mitral stenosis, plus severe regurgitation = regurgitant fraction ≥50%. |
| Term | What you need to know |
|---|---|
| ★ Aortic stenosis | Most common valve disease. >70 degenerative, <70 bicuspid. Harsh systolic crescendo-decrescendo, 2nd right space, to the carotids; softer with Valsalva, standing, handgrip; louder squatting, sitting forward. Forceful apex + delayed, weak carotid = severe. |
| ★ Aortic stenosis numbers | Severe = area <1.0 cm², mean gradient >40 mmHg, jet >4.0 m/s (“4, 40 and 1”). Survival: angina 5 y · syncope 3 y · heart failure 2 y (most common, worst). Symptomatic: 75% dead at 3 years. |
| ★ Aortic stenosis care | Preload dependent: avoid strenuous activity / competitive sports, dehydration; hypertension → avoid beta blockers and calcium channel blockers; angina → avoid nitrates. Surgery: severe + symptomatic systolic dysfunction, or bicuspid → transcatheter replacement; children / young adults → balloon valvuloplasty. All on echo → cardiology. |
| ★ Aortic regurgitation | High-pitched blowing DIASTOLIC, 3rd space / left upper sternal border, to the apex (the slide’s “holosystolic” is struck). Corrigan pulse (water hammer: rapid upstroke, rapid collapse), de Musset (head bobbing), wide pulse pressure. Root causes: Marfan, dissection, aortitis, hypertension. |
| Aortic regurgitation care | Echo finds the cause (root dilation, dissection) and shows the anterior mitral leaflet fluttering (the slide is right; “aortic leaflet” said in class is not). Chronic, preserved fraction → afterload reduction. Acute severe → emergency replacement (<24 h); if delayed, IV diuretics + nitroprusside. Falling fraction → surgery; untreated survival 2–3 y. Audible murmur → cardiology. |
| ★ Mitral stenosis | Rheumatic (most common; 80% women; ~20 y after the fever). Left atrium enlarges → atrial fibrillation → thromboembolism. Hemoptysis, hoarseness (Ortner), dysphagia. Low diastolic rumble at the apex after an opening snap, bell, left side; softer with Valsalva (slide 38’s “increased” is wrong). Severe = <1.0 cm², gradient >10, velocity >3.0. Loop diuretic → balloon valvotomy. |
| Mitral regurgitation | Backflow into the left atrium in systole. Acute: papillary muscle / chordae rupture, endocarditis. Holosystolic blowing at the apex → axilla; louder squatting, handgrip; softer standing, Valsalva. Severe = regurgitant fraction ≥50%. Surgery: ejection fraction <60% or end-systolic dimension >40 mm → clip, transcatheter or surgical replacement. |
| Mitral valve prolapse | Myxomatous; healthy women 15–30; mid-systolic click at the apex; echo: redundant leaflets >5 mm. Usually benign, no treatment; may progress to mitral regurgitation. |
| Term | What you need to know |
|---|---|
| Pulmonic stenosis | Almost always congenital (tetralogy of Fallot; carcinoid). Harsh mid-systolic ejection, left upper sternal border, louder on inspiration, split S2. Electrocardiogram: right axis deviation, right ventricular hypertrophy. Mild–moderate: none, 94% 20-y survival. Severe: diuretics + balloon valvuloplasty. On echo → cardiology. |
| ★ Pulmonic regurgitation | Iatrogenic = most common cause of SIGNIFICANT regurgitation (after valvotomy / valvuloplasty for outflow obstruction); pulmonary hypertension = the high-pressure cause, commonest overall (usually mild). Graham Steell: brief early diastolic decrescendo, 2nd left space. Usually incidental. Treat the cause; refer on echo or right heart failure. |
| Tricuspid stenosis | Rheumatic (with mitral disease), carcinoid; women. (Slide’s “congenital in the US” is wrong.) Right atrium → right ventricle blocked. Mid-diastolic rumble near the xiphoid, louder on inspiration; right upper quadrant pain, cold skin. Electrocardiogram: right atrial enlargement out of proportion. Low salt, diuretics, aldosterone antagonist; bioprosthetic replacement. (Suffusion sign not tested.) |
| ★ Tricuspid regurgitation | Most common = annular dilation from pulmonary hypertension; primary = endocarditis in intravenous drug users. Holosystolic, lower left sternal border, louder on inspiration (Carvallo) — that separates it from mitral regurgitation. Raised jugular pressure, venous thrill; severe: edema, ascites. Annuloplasty. |
| ★ Mechanical valve | Titanium and carbon → lifelong vitamin K antagonist (warfarin) — over no therapy and over antiplatelets. International normalized ratio: aortic 2.5 (2.0–3.0) · mitral 3.0 (2.5–3.5) · both 3.0. Surgery → bridge with heparin. |
| Biological valve | Pig or cow tissue → no anticoagulation beyond the immediate postoperative period; preferred when anticoagulation is contraindicated. By age: mechanical if younger, bioprosthetic / transcatheter if older (slide 74’s cut-offs are reversed; no age is keyed). |
| Term | What you need to know |
|---|---|
| Ischemia | Oxygen demand vs supply mismatch. Heart = 0.3% of body weight, 7% of oxygen use. Irreversible injury in 40–60 minutes. Wall motion on echo: hypokinesia (reduced), akinesia (none), dyskinesia (bulging). |
| ★ Arteries | Three main: right coronary, left anterior descending, circumflex. Right coronary supplies the atrioventricular node → complete heart block. Anterior interventricular artery = LAD (left anterior descending), the most common culprit (40–50%), then right coronary (30–40%), circumflex (15–20%). |
| Risk factors | Men ≥45, women ≥55; family history male <55 / female <65. Smoking = strong predictor in women <45. Plaque rupture → platelets + tissue factor → clotting cascade → fibrin. |
| ★ The pain | Substernal pressure, worse with exertion, not positional, relieved by nitroglycerin; Levine's sign = clenched fist over the sternum. Silent ischemia in diabetes, neuropathy, transplanted heart → dyspnea, nausea, fatigue. Referred: jaw, tooth, arm. |
| Workup | Every chest pain: chest radiograph + STAT electrocardiogram. Calcium score = risk stratification, not acute coronary syndrome. Abnormal nuclear stress test ⇒ cardiac catheterization. |
| ★ Risk scores | HEART = History, EKG (electrocardiogram), Age, Risk factors, Troponin (parts only). TIMI (Thrombolysis in Myocardial Infarction) 3 or higher → early invasive approach — the only score cut-off tested. |
| Term | What you need to know |
|---|---|
| ★ Troponin I | Standard: abnormal above 0.04 ng/mL. High-sensitivity: 12 ng/L women, 20 ng/L men (99th percentile). Rules OUT (who can go home); one means two (repeat, watch for a rise). Troponin I is heart-specific; smooth muscle has none. |
| Stable angina | Most common; with exertion, relieved by rest + nitroglycerin. Stress-test T-wave inversion; coronary angiography = gold standard. Beta blocker (calcium channel blocker if contraindicated), statin, aspirin ± clopidogrel. Call emergency medical services if unimproved 5 min after one dose or after 3 doses. |
| ★ Unstable angina vs the infarcts | Unstable angina: rest pain, inverted T waves, troponin normal. Non-ST-elevation infarction: ST depression >1 mm and/or T inversion in ≥2 consecutive leads + troponin elevated. ST-elevation: >1 mm in ≥2 consecutive leads; new left bundle branch block counts only with ongoing ischemia or instability (he taught it as an equivalent). |
| UA / NSTEMI treatment | Medical emergency: chewable aspirin, beta blocker, intravenous nitrates, dual antiplatelet ± anticoagulation. Oxygen only if SpO2 <91%. Then catheterization and angiography. |
| ★ Lead → artery | II, III, aVF = inferior = right coronary · I, aVL, V5–V6 = lateral = circumflex · V1–V4 = anterior/septal = LAD (V4 is anterior). Subendocardial → ST depression; transmural → ST elevation. Q waves = infarct already done. |
| ★ Posterior | ST depression in V1–V3 = posterior infarct (easy to miss) → record posterior leads V7–V9. |
| Term | What you need to know |
|---|---|
| ★ Time is muscle | Electrocardiogram within 10 min; door-to-balloon <90 min. Chewable aspirin, call the catheterization team, then P2Y12 antagonist + heparin; beta blocker if no bradycardia. Thrombolytics if intervention is 2+ hours away, within 30 min of arrival; tenecteplase most common. |
| ★ Right ventricular infarct | Right coronary occlusion reaching the right ventricle (15–30%; ST elevation V1, V4R): NO nitroglycerin — preload falls, shock. Also no nitroglycerin within 24 h of a phosphodiesterase inhibitor (ask women: pulmonary arterial hypertension). |
| Thrombolytic contraindications | Absolute: active bleeding, major surgery/trauma 4 weeks, hemorrhagic stroke in the previous year, unknown stroke 6 weeks, pregnancy, uncontrolled >190/100. |
| ★ Words have meaning | Catheterization = the tube in; angiography = dye + pictures; plain old balloon angioplasty = no stent; percutaneous coronary intervention = stent. Stopping dual antiplatelet therapy in the first 6 weeks → sudden stent THROMBOSIS (the slide’s “50% sudden in-stent restenosis” is wrong on both counts). Bypass: mammary/radial artery first, saphenous vein if not. |
| ★ After the infarct | Beta blockers improve survival with a reduced ejection fraction (not established if preserved; the deck says “across the board”); calcium channel blockers do not (diltiazem/verapamil: angina or rate control only, no mortality benefit; avoid in reduced ejection fraction). High-intensity statin for every acute coronary syndrome before discharge; ACE (angiotensin-converting enzyme) inhibitor if reduced function; warfarin only for an akinetic apex or left ventricular thrombus (slide: all large anterior infarcts). Dressler = pericarditis; cardiogenic shock more with left-sided. |
| ★ Sudden cardiac death | Most often ventricular fibrillation; the first sign of coronary disease in over 20%. |
| ★ Vasospastic (Prinzmetal) | Often <50, smoker, rest pain midnight–8 a.m., 5–15 min, transient ST elevation, normal coronaries. Gold standard: ergonovine/acetylcholine at angiography, relieved by nitroglycerin. Calcium channel blocker first-line; avoid nonselective beta blockers, aspirin, triptans. |
| Microvascular angina | Formerly cardiac syndrome X: angina + ST changes, normal coronaries, women, stress; diagnosis of exclusion (needs angiography); treated like coronary disease. |
| Term | What you need to know |
|---|---|
| 2022, not the deck | Tested on the 2022 guideline; slide 57 (2026 changes) = rotations only. Learn “mildly” reduced (not “moderately”), ≤40 / 41–49 / ≥50 (not <40 / >50), stage D = advanced (not “decompensated”), calcium channel blockers = avoid (no subclass ranking), beta blockers by class. Digitalis not keyed. |
| ★ Systolic vs diastolic | Systolic = squeeze fails: ischemic or dilated cardiomyopathy → reduced ejection fraction → normal or low pressure → third heart sound → pulmonary edema. Diastolic = relaxation fails: hypertrophic (hypertension) → preserved fraction → hypertension → fourth heart sound → peripheral then pulmonary edema. Add an elevated B-type natriuretic peptide = slam dunk. |
| ★ Normal values | Cardiac output 5–6 L/min. Normal ejection fraction ≥50% — the treatment line is 50 and above vs 49 and below. |
| Reduced | Ejection fraction ≤40%. |
| Mildly reduced | 41–49%, never previously ≤40%. |
| Preserved | ≥50%. |
| Improved | Was ≤40%, now >40% — history decides the label (30% → 46% is improved, not mildly reduced). |
| New York Heart Association class | I no symptoms · II symptoms with exertion · III with slight exertion · IV at rest. A grade of symptoms. |
| Stages A–D (natural history) | A at risk, normal heart · B pre-heart failure: structural disease, no symptoms (asymptomatic left ventricular hypertrophy = B, not A) · C symptomatic, past or current · D advanced. Never moves backward. |
| ★ Stage A / B therapy | Stage A with diabetes → sodium-glucose cotransporter 2 inhibitor, NOT a beta blocker (“it’ll be on your test”). Stage B adds ACE (angiotensin-converting enzyme) inhibitor (receptor blocker if intolerant) and beta blocker. |
| Term | What you need to know |
|---|---|
| ★ Clinical diagnosis | Signs and symptoms + an elevated B-type natriuretic peptide or objective congestion. “Clinical diagnosis requires congestion; congestion = edema.” |
| ★ Natriuretic peptide cut-offs | BNP (B-type natriuretic peptide): <100 rules out acute failure; 100–400 gray zone; >400 likely; >900 likely acute. NT-proBNP (N-terminal pro-B-type): <300 rules out; >125 likely if <75 years, >450 if >75. BNP is degraded by neprilysin, so sacubitril-valsartan alters it. |
| Which test answers what | Echocardiogram: structures, ejection fraction group, definitive for right-sided. Multigated acquisition scan: most accurate ejection fraction. Chest radiograph: effusion, cephalization, Kerley B lines, big heart. Metabolic panel: potassium, renal function. Troponin only if ischemia is suspected. |
| Left vs right | Left = 70–80%, pulmonary congestion, orthopnea, paroxysmal nocturnal dyspnea. Right = edema, jugular venous distension, hepatomegaly; most often from chronic left failure (also mitral stenosis, pulmonary arterial hypertension); worse prognosis. |
| ★ Reduced fraction therapy (all strong) | Angiotensin receptor-neprilysin inhibitor (class II–III) or ACE inhibitor / receptor blocker (II–IV) + beta blocker + mineralocorticoid receptor antagonist + sodium-glucose cotransporter 2 inhibitor + diuretics as needed. Hydralazine + isosorbide dinitrate for African American patients, class III–IV. |
| Mildly reduced & preserved | Diuretics as needed (strong); sodium-glucose cotransporter 2 inhibitor (moderate); the rest weak. “Very similar” to each other; different from reduced. |
| Avoid | Calcium channel blockers. Inotropes (dobutamine, milrinone) = intensive care only. |
| Defibrillator | Ejection fraction ≤35%, class II–III, on optimal therapy, life expectancy ≥1 year (the slide is right; he said “under a year”). After an acute event with fraction <35%: wearable vest → optimize + rehab → recheck echo. |
| High-output | Raised output from demand: anemia, hyperthyroidism, arteriovenous fistula (also obesity, chronic lung disease, cirrhosis, Paget disease). Treat the cause; diuretic. |