USMLE (Subject) / Cardiovascular (Lesson)

USMLE First Aid

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• Separation of the atria 1. Septum primum grows toward endocardial cushions (narrowing foramen primum) 2. Foramen secundum forms in septum primum (formamen primum disappears) 3. Septum secundum develops as foramen secundum maintains right-to-left shunt 4. Septum secundum covers most of the foramen secundum. The residual foramen is the foramen ovale.
• Patent foramen ovale - caused by failure of septum primum and septum secundum to fuse after birth - most are left untreated - can lead to paradoxical emboli (venous thromboemboli that enter systemic arterial circulation)
• Fetal-postnatal derivatives Allantois → urachus → Median umbilical ligament- Urachus is part of allantoic duct between bladder and umbilicus Ductus arteriosus → Ligamentum arteriosum Ductus venosus (bypasses hepatic circulation) → Ligamentum venosum Foramen ovale → Fossa ovalis Notochord → Nucleus pulposus Umbilical arteries → Medial umbilical ligaments Umbilical vein → Ligamentum teres hepatis (round ligament)- Contained in falciform ligament
• Splitting Normal splitting:- Inspiration → drop in intrathoracic pressure → ↑ venous return → ↑ RV filling → ↑ RV stroke volume → ↑ RV ejection time → delayed closure of pulmonic valve. ↓ pulmonary impedance (↑ capacity of the pulmonary circulation) also contributes to delayed closure of pulmonic valve. Wide splitting:- Seen in conditions that delay RV emptying (eg, pulmonic stenosis, right bundle branch block).- Causes delayed pulmonic sound (especially on inspiration). An exaggeration of normal splitting. Fixed splitting:- Heard in ASD - ASD → left-to-right shunt → ↑ RA and RV volumes → ↑ flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed. Paradoxical splitting:- In conditions that delay aortic valve closure (eg, aortic stenosis, left bundle branch block).- P2 sound occurs before delayed A2 sound. - Therefore, on inspiration, P2 closes later and moves closer to A2, thereby "paradoxically" eliminating the split (usually heard in expiration).
• Aortic stenosis Crescendo-decrescendo systolic ejection murmur and soft S2 (ejection click may be present). - LV >> aortic pressure during systole. Loudest at heart base; radiates to carotids.- Murmur louder with ↑ preload (eg, rapid squatting). - "Pulsus parvus et tardus" - pulses are weak with a delayed peak. - Can lead to syncope, angina, and dyspnea on exertion. - Most commonly due to age-related calcification in older patients (>60 years old) or in younger patients with early-onset calcification of bicuspid aortic valve.
• Mitral/tricuspid regurgitation - Holosystolic, high-pitched "blowing murmur."- Severity is indicated by an audible S3 gallop. Mitral - loudest at apex and radiates toward axilla.- MR is often due to ischemic heart disease (post-MI), MVP, LV dilatation. Tricuspid - loudest at tricuspid area.- TR is commonly caused by RV dilatation. - Rheumatic fever and infective endocarditis can cause either MR or TR.
• Mitral valve prolapse Late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae). - Most frequent valvular lesion, usually benign.- Best heard over apex. Loudest just before S2.- Squatting increases venous return and LV volume, helping to bring the valve leaflets into a more normal anatomic arrangement. This, in turn, decreases the degree of MVP, causing a delay in the onset of click during systole, and the systolic murmur becomes shorter or disappears. - Can predispose to infective endocarditis. - Can be caused by myxomatous degeneration (1° or 2° to connective tissue disease such as Marfan or Ehlers-Danlos syndrome), rheumatic fever, chordae rupture.
• Ventricular septal defect Holosystolic, harsh-sounding murmor.- Loudest at tricuspid area. Most common congenital cardiac defect.- Asymptomatic at birth, may manifest weeks later or remain asymptomatic throughout life.- Most self resolve; larger lesions may lead to LV overload and HF.- O2 saturation ↑ in RV and pulmonary artery.- Frequency: VSD > ASD > PDA.
• Aortic regurgitation Etiologies:- Congenital bicuspid aortic valve- Postinflammatory (eg, rheumatic heart disease, endocarditis)- Aortic root dilation (eg, Marfan syndrome, syphilis) Clinical findings:- High-pitched "blowing" early diastolic decrescendo murmur- Widened pulse pressure (↑ SBP & ↓ DBP)- Rapid rise-rapid fall ("water-hammer") pulsation- Abrupt carotid distension & collapse, "pistol-shot" femoral pulses- Long diastolic murmur, hyperdynamic pulse, and "head-bobbing" when chronic and severe.
• Mitral stenosis - Follows opening snap (OS; due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips). - Delayed rumbling mid-to-late diastolic murmur (↓ interval between S2 and OS correlates with ↑ severity). - LA >> LV pressure during diastole. - Often a late and highly speific sequela of rheumatic fever.- Chronic MS can result in LA dilatation → dysphagia/hoarseness via compression of esophagus/left recurrent laryngeal nerve, respectively.
• Patent ductus arteriosus In fetal period, shunt is right to left (normal). In neonatal period, ↓ pulmonary vascular resistance → shunt becomes left to right → progressive RVH and/or LVH and HF. - Continuous, "machine-like" murmur.- Best heard at left infraclavicular area.- Loudest at S2.- Often due to congenital rubella or prematurity. - Patency is maintained by PGE synthesis and low O2 tension.- Indomethacin ends patency of PDA. - Uncorrected PDA can eventually result in late cyanosis in the lower extremities.
• Torsades de pointes Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG- Can progress to ventricular fibrillation (VF). Cause:- Long QT interval predisposes to torsades de pointes- Drugs: Antiarrhythmics (class IA, III), macrolide antibiotics, antipsychotics (eg, haloperidol), antidepressants (eg, TCAs), antiemetics (eg, ondansetron)- Electrolyte abnormalities: ↓ K+, ↓ Mg2+- Congenital abnormalities Treatment includes magnesium sulfate.
• Congenital long QT syndrome Inherited disorder of myocardial repolarization, typically due to ion channel defects.- Most common forms are due to genetic mutations in K+ channel proteins that contribute to the outward-rectifying potassium current. - ↑ risk of sudden cardiac death (SCD) due to torsades de pointes. Romano-Ward syndrome: - Autosomal dominant- Pure cardiac phenotype (no deafness)- Associated with ventricular tachyarrhythmias Jervell and Lange-Nielson syndrome: - Autosomal recessive- Sensorineural deafness- Associated with ventricular tachyarrhythmias
• Brugada syndrome - Autosomal dominant disorder most common in Asian males.- Affects sodium channels and disturbs repolarization. - ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3. - ↑ risk of ventricular tachyarrhythmias and SCD. - Prevent SCD with implantable cardioverter-defibrillator (ICD).
• Wolff-Parkinson-White syndrome - Most common type of ventricular pre-excitation syndrome. - Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node → ventricles begin to partially depolarize earlier → characteristic delta wave with widenened QRS complex and shortened PR interval. - May result in reentry circuit → supraventricular tachycardia.
• Atrial fibrillation - Chaotic and erratic baseline with no discrete P waves in between irregularly spaced QRS complexes.- Ventricular response is dependent on the transmission through the AV node, and thus, the AV node refractory period. - Irregularly irregular heartbeat. - Most common risk factors include hypertension and coronary artery disease (CAD). - Can lead to thromboembolic events, particularly stroke. Treatment: anticoagulation, rate control, rhythm control, and/or cardioversion.
• Atrial flutter A rapid succession of identical, back-to-back atrial depolarization waves - "Sawtooth" appearance of the flutter waves. - Treat like atrial fibrillation. Definitve treatment is catheter ablation.
• Right-to-left shunts Early cyanosis ("blue babies"). Often diagnosed prenatally or become evident immediately after birth. Usually require surgical treatment and/or maintenance of a PDA. 1. Truncus arteriosus2. Transposition of the great vessels3. Tricuspid atresia4. Tetralogy of Fallot5. Total anomalous pulmonary venous return
• Persistent truncus arteriosus Truncus arteriosus fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation. Most patients have accompanying VSD.
• Transposition of great vessels Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior) → separation of systemic and pulmonary circulations.- Due to failure of the aorticopulmonary septum to spiral. - Not compatible with life unless a shunt is present to allow mixing of blood (eg, VSD, PDA, or patent foramen ovale). Risk factors: - Infants born to diabetic mothers- Maternal alcohol consumption, age >40 years Without servical intervention, most infants die within the first few months of life.
• Tricuspid atresia Absence of tricuspid valve and hypoplastic RV. Requires both ASD and VSD for viability.
• Tetrology of Fallot Caused by anterosuperior displacement of the infundibular septum.- Most common cause of early childhood cyanosis. 1. Pulmonary infundibular stenosis (most important determinant for prognosis)2. Right ventricular hypertrophy – boot-shaped heart on CXR3. Overriding aorta4. VSD Pulmonary stenosis forces right-to-left flow across VSD → RVH, "tet spells" (often caused by crying, fever, and exercise due to exacerbation of RV outflow obstruction). Squatting: ↑ SVR, ↓ right-to-left shunt, improves cyanosis. Treatment: early surgical correction
• Ebstein anomaly Characterized by the displacement of tricuspid valve leaflets downward into RV, artificially "atrializing" the ventricle. - Associated with tricuspid regurgitation, accessory conduction pathways, and right-sided HF. - Can be caused by lithium exposure in utero.
• Eisenmenger syndrome Uncorrected left-to-right shunt (VSD, ASD, PDA) → ↑ pulmonary blood flow → pathologic remodeling of vasculature → pulmonary arterial hypertension. - RVH occurs to compensate → shunt becomes right to left. - Causes late cyanosis, clubbing, and polycythemia.
• Coarctation of the aorta Aortic narrowing near insertion of ductus arteriosus ("juxtaductal").- Associated with bicuspid aortic valve, other heart defects, and Turner syndrome. - Hypertension in upper extremities and weak, delayed pulse in lower extremities (brachial-femoral delay). - With age, intercostal arteries enlarge due to collateral circulation; arteries erode ribs → notched appearance on CXR. - Complications include HF, ↑ risk of cerebral hemorrhage (berry aneurysms), aortic rupture, and possible endocarditis.
• Congenital cardiac defect associations Alcoholic exposure in utero → VSD, PDA, ASD, tetralogy of Fallot Congenital rubella → PDA, pulmonary artery stenosis, septal defects Down syndrome → AV septal defect (endocardial cushion defect), VSD, ASD Infant of diabetic mother → Transposition of great vessels, VSD Marfan syndrome → MVP, thoracic aortic aneurysm and dissection, aortic regurgitation Prenatal lithium exposure → Ebstein anomaly Turner syndrome → Bicuspid aortic valve, coarctation of aorta Williams syndrome → Supravalvular aortic stenosis 22q11 syndromes → Truncus arteriosus, tetralogy of Fallot
• Hypertension Defined as persistent systolic ≥140 mmHg and/or diastolic BP ≥90 mmHg. Risk factors: ↑ age, obesity, diabetes, physical inactivity, excess salt intake, excess alcohol intake, cigarette smoking, family history; African American > Caucasian > Asian. - 90% of hypertension is 1° (essential) and related to ↑ CO or ↑ TPR.- 10% is mostly 2° to renovascular disease such as fibromuscular dysplasia (characteristic "string of beads" appearance of renal artery) and atherosclerotic renal artery stenosis or 1° hyperaldosteronism. Hypertensive urgency – severe (≥180/≥120 mmHg) hypertension without acute end-organ damage.Hypertensive emergency – severe hypertension with evidence of acute end-organ daamge (eg, encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia). Predisposes to CAD, LHF, HF, atrial fibrillation; aortic dissection, aortic aneurysm; stroke; chronic kidney disease (hypertensive nephropathy); retinopathy.
• Diagnosis of myocardial infarction - In the first 6 hours, ECG is the gold standard. - Troponin I rises after 4 hours (peaks at 24 hr) and is ↑ for 7-10 days; more specific than other protein markers. - CK-MB rises after 6-12 hours (peaks at 16-24 hr) and is predominantly found in myocardium but can also be released by skeletal muscle. Useful in diagnosing reinfarction following acute MI because levels return to normal after 48 hours. - Large MIs lead to greater elevations in troponin I and CK-MB.  - ECG changes can include ST elevation (STEMI, transmural infarct), ST depression (NSTEMI, subendocardial infarct), hyperacute (peaked) T waves, T-wave inversion, new left bundle branch block, and pathologic Q waves or poor R wave progression.
• Myocardial infarction complications Cardiac arrhythmia: Important cause of death before reaching hospital and within the first 24 hours post-MI. Postinfarction fibrinous pericarditis: Occurs 1-3 days after MI. Friction rub. Papillary muscle rupture: Occurs 2-7 days after MI. Posteromedial papillary muscle rupture ↑ risk due to single blood supply from posterior descending artery. Can result in severe mitral regurgitation. Interventricular septal rupture: Occurs 3-5 days after MI. Macrophage-mediated degradation → VSD → ↑ O2 saturation and pressure in RV. Ventricular pseudoaneurysm formation: Occurs 3-14 days after MI. Contained free wall rupture; ↓ CO, risk of arrhythmia, embolus from mural thrombus. Ventricular free wall rupture: Occurs 5-14 days after MI. Free wall rupture → cardiac tamponade. LV hypertrophy and previous MI protect against free wall rupture. Acute form usually leads to sudden death. True ventricular aneurysm: Occurs 2 weeks to several months after MI. Outward bulge with contraction ("dyskinesia"), associated with fibrosis. Dressler syndome: Occurs several weeks after MI. Autoimmune phenomenon resulting in fibrinous pericarditis. LV failure and pulmonary edema: Can occur 2° to LV infarction, VSD, free wall rupture, papillary muscle rupture with mitral regurgitation.
• Dilated cardiomyopathy Most common cardiomyopathy (90% of cases). - Most often idiopathic or familial (50%).- Coronary or valvular heart disease- Chronic alcohol abuse- Wet beriberi (thiamine deficiency)- Coxsackie B viral myocarditis- Chronic cocaine abuse- Chagas disease- Drugs: Anthracyclines such as doxorubicin/daunorubicin, transtuzumab- Hemochromatosis- Sarcoidosis- Thyrotoxicosis- Peripartum cardiomyopathy Findings: HF, S3, systolic regurgitant murmur, dilated heart on echocardiogram, balloon appearance of heart on CXR.- Leads to systolic dysfunction (reduced left-ventricular ejection fraction).- Displays eccentric hypertrophy (sarcomeres added in series). Takotsubo cardiomyopathy: "broken heart syndrome" – ventricular apical ballooning likely due to increased sympathetic stimulation (eg, stressful situations). Treatment: Na+ restriction, ACE inhibitors, β-blockers, diuretics, digoxin, ICD, heart transplant.
• Hypertrophic obstructive cardiomyopathy 60-70% of cases are familial, autosomal dominant (commonly due to mutations in genes encoding sarcomeric proteins, such as myosin binding protein C and β-myosin heavy chain).- Can be associated with Friedreich ataxia - Causes syncope during exercise and may lead to sudden death in young athletes due to ventricular arrhythmia. - Findings: systolic murmur. Increases with Valsalva maneuver and standing. Decreases with hand grip, squatting.- S4 gallop due to a thickened, non-compliant ventricle.- May see mitral regurgitation due to impaired mitral valve closure.- Diastolic dysfunction ensues.- Marked ventricular concentric hypertrophy, often septal predominance. Myofibrillar disarray and fibrosis.- Physiology of HOCM – asymmetric septal hypertrophy and systolic anterior motion of mitral valve → outflow obstruction → dyspnea, syncope.- Obstruction exacerbated by ↓ preload or afterload (Reduction of afterload increases the pressure gradient over the obstruction. In this situation, blood can only be ejected at higher pressures, requiring the heart to contract more strongly. This may increase the obstruction of the ventricular outflow tract.) Treatment: cessation of high-intensity athletics, β-blocker or non-dihydropyridine Ca2+ channel blockers (eg, verapamil). ICD if high risk.- The LVOT obstruction worsens with decreased LV volume, which can be caused by reduction in cardiac preload and/or afterload. Therefore, positive-inotropic and afterload-reducing/preload-reducing drugs (vasodilators or diuretics, ACE inhibitors, NO) are contraindicated.
• Restrictive/infiltrative cardiomyopathy Major causes include:- Sarcoidosis- Amyloidosis- Postradiation fibrosis- Endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children)- Hemochromatosis (although dilated cardiomyopathy is more common)Löffler endocarditis – associated with hypereosinophilic syndrome; histology shows eosinophilic infiltrates in myocardium. - Diastolic dysfunction ensues- Can have low-voltage ECG despite thick myocardium (especially in amyloidosis)- Histology: Endomyocardial fibrosis
• Heart failure Clinical syndrome of cardiac pump dysfunction → congestion and low perfusion.- Symptoms include dyspnea, orthopnea, fatigue.- Signs include S3 heart sound, rales, jugular venous distention (JVD), pitting edema. Systolic dysfunction – reduced EF, ↑ EDV, ↓ contractility often 2° to ischemia/MI/dilated cardiomyopathy.Diastolic dysfunction – preserved EF, normal EDV, ↓ compliance (↑ EDP) often 2° to myocardial hypertrophy. - Right HF most often results from left HF.- Cor pulmonale refers to isolated right HF due to pulmonary cause. - ACE inhibitors or angiotensin II receptor blockers, β-blockers, and spironolactone ↓ mortality.- Thiazide or loop diuretics are used mainly for symptomatic relief.- Hydralazine with nitrate therapy improves symptoms and mortality in select patients.
• Left heart failure Orthopnea – Shortness of breath when supine: ↑ venous return from redistribution of blood (immediate gravity effect) exacerbates pulmonary vascular congestion. Paroxysmal nocturnal dyspnea – Breathless awakening from sleep: ↑ venous return from redistribution of blood, reabsorption of peripheral edema. Pulmonary edema – ↑ pulmonary venous pressure → pulmonary venous distension and transudation of fluid. Presence of hemosiderin-laden macrophages ("HF" cells) in lungs.
• Right heart failure Hepatomegaly (nutmeg liver): ↑ central venous pressure → ↑ resistance to portal flow. Rarely, leads to "cardiac cirrhosis." Jugular venous distention: ↑ venous pressure. Peripheral edema: ↑ venous pressure → fluid transudation.
• Bacterial endocarditis Acute – S aureus (high virulence). Large vegetations on normal valves. Rapid onset.Subacute – viridans streptococci (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequelae of dental procedures. Gradual onset.- S epidermidis on prosthetic valves or pacemakers.- Enterococci following GI or GU procedures.- S bovis (gallolyticus) is present in colon cancer.- If culture ⊝, most likely Coxiella burnetti, Bartonella, HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella). - Mitral valve is most frequently involved. - Tricuspidal valve endocarditis is associated with IV drug abuse. Associated with S aureus, Pseudomonas, Candida. Symptoms:- Fever (most common), new murmur- Roth spots (round white spots on retina surrounded by hemorrhage)- Osler nodes (tender raised lesions on finger or toe pads; may embolic or immune complex-mediated)- Janeway lesions (small, painless, erythematous lesions on palm or sole)- Splinter hemorrhages on nail bed- Associated with glomerulonephritis, septic arterial or pulmonary emboli. Nonbacterial (marantic/thrombotic) endocarditis: Rare, non-infectious form of endocarditis due to sterile platelet thrombus formation on the heart valves.- Associated with underlying malignancy, hypercoagulable state, or rheumatologic conditions (eg, SLE, rheumatoid arthritis).- Vegetations composed of immune complexes, mononuclei, interwoven fibrin- Libman-Sacks endocarditis: describes large vegetations, also referred to as verrucous Treatment:- S epidermidis: Vancomycin (assume methicillin-resistance until proven otherwise)- Native-valve endocarditis due to methicillin-sensitive staphylococci: Nafcillin or oxacillin
• Rheumatic fever A consequence of pharyngeal infection with group A β-hemolytic streptococci.- Late sequelae include rheumatic heart disease, which affects heart valves – mitral > aortic >> tricuspid (high-pressure valves affected most). - Early lesion is mitral valve regurgitation.- Late lesion is mitral stenosis. - Associated with Aschoff bodies (granuloma with giant cells)- Anitschkow cells (enlarged macrophages with wavy, rod-like nucleus)- ↑ anti-streptolysin O (ASO) titers Jones (major criteria): Joint (migratory polyarthritis) ♥ (carditis)Nodules in skin (subcutaneous)Erythema marginatum (evanescent rash with ring margin)Syndeham chorea - Immune mediated (type II hypersensitivity); not a direct effect of bacteria.- Antibodies to M protein cross-react with self antigens (molecular mimicry). Treatment/prophylaxis: penicillin
• Acute pericarditis Inflammation of the pericardium Etiologies:- Infectious: Most commonly viral (eg, coxsackie), bacterial (eg, tuberculosis), toxoplasmosis- Myocardial infarction: within 1-3 days → post-infarction fibrinous pericarditis; within weeks to months → Dressler syndrome- Postoperative- Autoimmune: SLE, rheumatoid arthritis- Other: Uremia, neoplasia, radiation therapy Presentation:- Low-grade intermittent fever, dyspnea, tachypnea, non-productive cough- Sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward- Pericardial friction rub: high-pitched scratching sound heard best during expiration while patient is sitting up and leaning forward- Often complicated by pericardal effusion. - Chronic pericarditis: ↑ JVP (with prominent x and y descents), pericardial knock, pulsus paradoxus, Kussmaul sign - ECG changes include widespread ST-segment elevation and/or PR depression
• Kussmaul sign - ↑ in JVP on inspiration instead of a normal ↓. - Inspiration → negative intrathoracic pressure not transmitted to heart → impaired filling of right ventricle → blood backs up into venae cava → JVD. - Seen with constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors.
• Cardiac tamponade Compression of the heart by fluid (eg, blood, effusions in pericardial space) → ↓ CO.- Equilibration of diastolic pressures in all 4 chambers. Findings:- Beck triad: Hypotension, distended neck veins, distant heart sounds- ↑ HR- ECG shows low-voltage QRS and electrical alternans (due to "swinging" movement of heart in large effusion) Pulsus paradoxus – ↓ in amplitude of systolic BP by >10 mmHg during inspiration. Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup.
• Pulsus paradoxus ↓ in amplitude of systolic BP by > 10 mm Hg during inspiration Seen in:- cardiac tamponade- asthma- obstructive sleep apnea- pericarditis- croup
• Heart embryology Truncus arteriosus → Ascending aorta and pulmonary trunk Bulbus cordis → Smooth parts (outflow tract) of left and right ventricles Endocardial cushion → Atrial septum, membranous intraventricular septum; AV and semilunar valves Primitive atrium → Trabeculated part of left and right atriaPrimitive ventricle → Trabeculated part of left and right ventricles Primitive pulmonary vein → Smooth part of left atrium Left horn of sinus venosus → Coronary sinusRight horn of sinus venosus → Smooth part of right atrium (sinus venarum) Right common cardinal vein and right anterior cardinal vein → Superior vena cava
• Heart morphogenesis First functional organ in vertebrate embryos; beats spontaneously by 4 weeks of development. Cardiac looping: Primary heart tube loops to establish left-right polarity; begins in week 4.- Defect in left-right dynein can lead to dextrocardia, as seen in Kartagener syndrome. Septation of the atria:1. Septum primum grows toward endocardial cushions, narrowing foramen primum2. Foramen secundum forms in septum primum 3. Septum secundum develops as foramen secundum maintains right-to-left shunt4. Septum secundum expands and covers most of the foramen secundum = foramen ovale5. Remaining portion of septum primum forms the valve of foramen ovale Patent foramen ovale – caused by failure of septum primum and septum secundum to fuse after birth; most are left untreated. Can lead to paradoxical emboli, similar to those resulting from an ASD. Septation of ventricles:1. Muscular interventricular septum forms2. Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum3. Growth of endocardial cushions separates atria from ventricles and contributes to atrial septation and membranous portion of the interventricular septum. Ventricular septal defect – most common congenital cardiac anomaly, usually occurs in membranous septum. Outflow tract formation: Neural crest and endocardial cell migrations → truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum → ascending aorta and pulmonary trunk.Conotruncal abnormalities associated with failure of neural crest cells to migrate:- Transposition of great vessels- Tetrology of Fallot- Persistent truncus arteriosus Valve development: - Aortic/pulmonary: derived from endocardial cushions of outflow tract- Mitral/tricuspid: derived from fused endocardial cushions of the AV canal- Valvular anomalies may be stenotic, regurgitant, atretic (eg, tricuspid atresis), or displaced (eg, Ebstein anomaly)
• Fetal circulation Blood in umbilial vein has a PO2 of ~30 mmHg and is ~80% saturated with O2. Umbilical arteries have low O2 saturation. 3 important shunts:1. Blood entering fetus through the umbilical vein is conducted via the ductus venosus into the IVC, bypassing hepatic circulation.2. Most of the highly oxygenated blood reaching the heart through the IVC is directed through the foramen ovale and pumped into the aorta to supply the head and body.3. Deoxygenated blood from the SVC passed through the RA → RV → main pulmonary artery → ductus arteriosus → descending aorta; shunt is due to high fetal pulmonary artery resistance. At birth, infant takes a breath → ↓ resistance in pulmonary vasculature → ↑ left atrial pressure vs right atrial pressure → foramen ovale closes (now called fossa ovalis); ↑ O2 (from respiration) and ↓ in prostaglandins (from placental separation) → closure of ductus arteriosus. Indomethacin helps close PDA → ligamentum arteriosum (remnant of ductus arteriosus).Prostaglandins E1 and E2 keep PDA open.
• Anatomy of the heart SA node is commonly supplied by right coronary artery (RCA); AV node supplied by PDA. Infarct may cause nodal dysfunction (bradycardia or heart block). Right-dominant circulation (85%): Posterior descending artery (PDA) arises from RCA.Left-dominant circulation (8%): PDA arises from left circumflex artery (LAD).Codominant circulation (7%): PDA arises from both LCX and RCA. - Coronary artery occlusion most commonly occurs in the left anterior descending artery (LAD). - Coronary blood flow peaks in early diastole. The most posterior part of the heart is the left atrium; enlargement can cause dysphagia (due to compression of the esophagus) or hoarseness (due to compression of the left recurrent laryngeal nerve). Pericardium consists of 3 layers (from outer to inner)- Fibrous pericardium- Parietal layer of serous pericardium- Visceral layer of serous pericardiumPericardial cavity lies between parietal and visceral layers.Pericardium innervated by phrenic nerve. Pericarditis can cause referred pain to the shoulder.
• Cardiac output CO = stroke volume (SV) x heart rate (HR) Fick principle:CO = rate of O2 consumption/(arterial O2 content - venous O2 content) - During the early stages of exercise, CO is maintained by ↑ HR and ↑ SV. During the late stages, CO is maintained by ↑ only (SV plateaus).- Diastole is preferentially shortened with ↑ HR; less filling time → ↓ CO (eg, ventricular tachycardia). Mean arterial pressure (MAP) = CO x total peripheral resistance (TPR)MAP = 2/3 diastolic pressure + 1/3 systolic pressure Pulse pressure = systolic pressure - diastolic pressurePulse pressure is proportional to SV, inversely proportional to arterial compliance.- ↑ pulse pressure in hyperthyroidism, aortic regurgitation, aortic stiffening (isolated systolic hypertension in elderly), obstructive sleep apnea (↑ sympathetic tone), anemia, exercise.- ↓ pulse pressure in aortic stenosis, cardiogenic shock, cardiac tamponade, advanced heart failure (HF).
• Cardiac output variables Stroke volume ↑ with: ↑ contractility, ↑ preload, ↓ afterload Preload: approximated by ventricular end-diastolic volume (EDV)- Depends on venous tone and circulating blood volume.- Venous vasodilators (eg, nitroglycerin) ↓ preload. Afterload: approximated by mean arterial pressure (MAP)- ↑ afterload → ↑ pressure → ↑ wall tension per Laplace's law.- LV compensates for ↑ afterload by thickening (hypertrophy) in order to ↓ wall tension.- Arterial vasodilators (eg, hydralazine) ↓ afterload.- ACE inhibitors and ARBs ↓ both preload and afterload.- Chronic hypertension (↑ MAP) → LV hypertrophy. Myocardial oxygen demand is ↑ by: ↑ contractility, ↑ afterload, ↑ heart rate, ↑ diameter of ventricle (↑ wall tension).- Wall tension = pressure x radius Ejection fraction = SV/EDV 
• Contractility Contractility (and SV) ↑ with:- Catecholamine stimulation via β1 receptor: → Ca2+ channels phosphorylated → ↑ Ca2+ entry → Ca2+ induced Ca2+ release and ↑ Ca2+ storage in sarcoplasmic reticulum→ Phospholamban phosphorylation → active Ca2+ ATPase → Ca2+ storage in SR- ↑ intracellular Ca2+- ↓ extracellular Na+ (↓ activity of Na+/Ca+ exchanger)- Digitalis (blocks Na+/K+ pump → ↑ intracellular Na+ → ↓ Na+/Ca+ exchanger activity → ↑ intracellular Ca2+) Contractility (and SV) ↓ with:- β1-blockade (↓ cAMP)- HF with systolic dysfunction- Acidosis- Hypoxemia/hypercapnia - Non-dihydropyridine Ca2+ channel blockers
• Starling curve Force of contraction is proportional to end-diastolic length of cardiac muscle fiber (preload). ↑ contractility with catecholamines, positives inotropes (eg, digoxin). ↓ contractility with loss of myocardium (eg, MI), β-blockers, non-dihydropyridine Ca2+ channel blockers, dilated cardiomyopathy.
• Heart sounds S1 – mitral and tricuspid valve closure. Loudest at mitral area. S2 – aortic and pulmonary valve closure. Loudest at upper sternal border. S3 – in early diastole during rapid ventricular filling phase. Associated with ↑ filling pressure (eg, mitral regurgitation, HF) and more common in dilated ventricles (but can be normal in children, young adults, and pregnant women). S4 – in late diastole ("atrial kick"). Best heard at apex with patient in left lateral decubitus position. High atrial pressure. Associated with ventricular noncompliance (eg, hypertrophy).Left atrium must push against stiff LV wall. Consider abnormal, regardless of patient age.

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