Cardiology Flashcards
Truncus Arteriosus gives rise to…
Ascending Aorta and pulmonary trunk
Bulbus Cordis gives rise to…
smooth parts (outflow tract) of left and right ventricles
Primitive ventricle gives rise to…
trabeculated left and right ventricles
Primitive atria gives rise to…
trabeculated left and right atria
Left horn of sinus venosus gives rise to…
coronary sinus
Right horn of sinus venosus gives rise to…
smooth part of right atrium
right common cardinal vein and right anterior cardinal vein gives rise to…
SVC
Embryology of truncus arteriosus
1) neural crest migration
2) truncal and bulbar ridges that spiral and fuse to form the aorticopulmonary (AP) septum
3) Ascending aorta and pulmonary trunk
Pathology of Truncus Arteriosus
1) transposition of great vessels- failure to spiral
2) tetralogy of Fallot- skewed AP septum development
3) persistent Truncus Arteriosus- partial AP septum development
Interventricular septum development
1) Muscular ventricular septum forms. Opening is called interventricular foramen.
2) AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular foramen.
3) Growth of endocardial cushions separates atria from ventricles and contributes to both atrial separation and membranous portion of the interventricular septum
Pathology of interventricular septum
1) improper neural crest migration into the truncus arteriosus (TA) can result in transposition of the great arteries or a persistent TA
2) membranous septal defect causes an initial left to right shunt which later reverses to a right to left shunt due to the onset of pulmonary hypertension (Eisenmenger’s syndrome)
Interatrial Septum development
1) Foramen Primum narrows as septum primum grows toward endocardial cushions.
2) Perforations in septum primum form foramen secundum (foramen primum disappears)
3) Foramen secundum maintains right to left shunt as septum secundum begins to grow
4) Septum secundum contains a permanent opening (foramen ovale)
5) Foramen secundum enlarges and upper part of septum primum degenerates
6) Remaining portion of septum primum forms valve of foramen ovale.
7) Septum secundum and septum primum fuse to form the atrial septum
8) Foramen ovale usually closes soon after birth because of increased left atrial pressure.
Pathology of Interatrial Septum
Patent foramen ovale caused by failure of the septum primum and septum secundum to fuse after birth
Fetal Erythropoiesis
1) Yolk Sac: 3-10 weeks
2) Liver: 6 weeks to birth
3) Spleen: 15-30 weeks
4) Bone Marrow: 22 weeks to adult
Fetal Circulation (shunts)
1) blood entering the fetus through the umbilical vein is conducted via the ductus venosus into the IVC to bypass the hepatic circulation
2) Most oxygenated blood reaching the heart via the IVC is diverted through the foramen ovale and pumped out the aorta to the head and body
3) Deoxygenated blood entering the RA from the SVC enters the RV, is expelled into the pulmonary artery and then passes through the ductus arteriosus into the descending aorta.
Umbilical Vein
Ligamentum teres hepatis, contained in falciform ligament
Umbilical arteries
medial umbilical ligaments
ductus arteriosus
ligamentum arteriosum
ductus venosus
ligamentum venosum
foramen ovale
fossa ovalis
allantois
urachus-median umbilical ligament; the urachus is part of the allantoic duct between the bladder and the umbilicus. Urachal cyst or sinus is a remnant.
Notochord
Nucleus pulposus of intervertebral disc
SA and AV nodes are supplied by…
Right coronary artery (RCA)
Right dominant circulation
85%; posterior descending artery (PD) arises from RCA
Left dominant circulation
8%; PD arises from left circumflex coronary artery (LCX)
Codominant circulation
7%; PD arises from both LCX and RCA
Most common coronary artery occlusion?
Left Anterior Descending artery (LAD)
When do coronary arteries fill?
During Diastole
LCX supplies…
lateral and posterior walls of the left ventricle
LAD supplies…
anterior 2/3 of interventricular septum, anterior papillary muscle and anterior surface of left ventricle
PD supplies…
posterior 1/3 of interventricular septum and posterior walls of ventricles
Most posterior part of the heart?
Left atrium; enlargement can cause dysphagia due to compression of the esophagus or hoarseness due to compression of the left recurrent laryngeal nerve
Transesophageal echocardiography
useful for diagnosing left atrial enlargement, aortic dissection and thoracic aortic aneurysm
stroke volume is affected by…
contractility, afterload and preload. Increased SV when increased preload, decreased afterload or increased contractility
Contractility increases with…
1) catecholamines (increased activity of Ca pump in sarcoplasmic reticulum)
2) increased intracellular Ca
3) decreased extracellular Na (decreased activity of Na/Ca exchanger)
4) Digitalis (blocks Na/K pump which increases intracellular Na and decreases activity of Na/Ca exchanger which then increases intracellular Ca)
Contractility decreases with…
1) Beta 1 blockade (decreases cAMP)
2) heart failure (systolic dysfunction)
3) acidosis
4) hypoxia/hypercapnea
5) Non-dihydropyridine Ca channel blockers
Myocardial O2 demand is increased by ?
1) increased afterload
2) increased contractility
3) increased heart rate
4) increased heart size (increased wall tension)
Inspiration
increased intensity of right heart sounds
expiration
increased intensity of left heart sounds
Hand grip (increased systemic vascular resistance)
increased intensity of MR, AR, VSD, MVP murmurs; decreased intensity of AS, hypertrophic cardiomyopathy murmurs
Valsalva (decreased venous return)
decreased intensity of most murmurs; increased intensity of MVP, hypertrophic cardiomyopathy murmurs
Rapid Squatting (increased venous return, increased preload, increased afterload with prolonged squatting)
decreased intensity of MVP, hypetrophic cardiomyopathy murmurs
Systolic heart sounds
aortic/pulmonic stenosis, mitral/ tricuspid regurgitation, ventricular septal defect
Diastolic heart sounds
aortic/pulmonic regurgitation, mitral/tricuspid stenosis
What can you hear in aortic area?
1) aortic stenosis
2) flow murmur
3) aortic valve sclerosis
What can you hear in left sternal border?
1) aortic regurgitation
2) pulmonic regurgitatio
3) hypertrophic cardiomyopathy
what can you hear in pulmonic area?
1) pulmonic stenosis
2) flow murmur (atrial septal defect, patent ductus arterious)
What can you hear in tricuspid area?
1) tricuspid regurgitation
2) ventricular septal defect
3) tricuspid stenosis
4) atrial septal defect
What can you hear in mitral area?
1) mitral regurgitation
2) mitral stenosis
Mitral regurgitation
high pitched “blowing murmur”; loudest of apex and radiates toward axilla. Enhanced by maneuvers that increase TPR (squatting or hand grip) or LA return (expiration). It is often due to ischemic heart disease, mitral valve prolapse or LV dilation
Tricuspid regurgitation
It is loudest at tricuspid area and right sternal border. Enhanced by maneuvers that increase RA return (inspiration). It can be caused by RV dilation. Rheumatic fever and infective endocarditis can cause either MR or TR
Aortic Stenosis
“Pulsus Parvus et tardus” Pulses are weak with a delayed peak. Can lead to Syncope, Angina and Dyspnea on exertion. Often due to age related calcific aortic stenosis or bicuspid aortic valve.
VSD
Harsh sounding murmur. Loudest at tricuspid area, accentuated with hand grip maneuver due to increased afterload.
Mitral Valve Prolapse (MVP)
Late systolic crescendo murmur with midsystolic click due to sudden tensing of chordae tendinae. Most frequent valvular lesion, best heard over apex, loudest at S2. Usually benign, can predispose to infective endocarditis. It can be caused by myxomatous degeneration, rheumatic fever or chordae rupture. Enhanced by maneuvers that decrease venous return (standing or Valsalva).
Aortic Regurgitation (AR)
Immediate high pitched “blowing” diastolic decrescendo murmur. Wide pulse pressure when chronic; can present with bounding pulses and head bobbing. Often due to aortic root dilation, bicuspid aortic valve, endocarditis or rheumatic fever. Increased murmur during hand grip. Vasodilators decrease intensity of murmur.
Mitral Stenosis (MS)
Follows opening SNAP due to abrupt halt in leaflet motion in diastole after rapid opening due to fusion at leaflet tips. Delayed rumbling late diastolic murmur. Often occurs secondary to rheumatic fever. Chronic MS can result in LA dilation. Enhanced by maneuvers that increase LA reurn (expiration)
PDA
Continuous machine-like murmur. Loudest at S2. Often due to congenital rubella or prematurity. Best heard at left infraclavicular area.
Atrial Fibrillation
Chaotic and erratic baseline with no discrete P waves in between irregularly placed QRS complexes. Can result in atrial stasis and lead to stroke. Treatment includes rate control, anticoagulation and possible cardioversion.
Atrial Flutter
rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves.
Ventricular fibrillation
completely erratic rhythm with no identifiable waves. Fatal Arrythmia without immediate CPR and defibrillation
Right to Left Shunts (early Cyanosis)- Blue babies
5 Ts
1) tetralogy of fallot (most common cause of early cyanosis)
2) Transposition of great vessels
3) Persistent Truncus Arteriosus
4) Tricuspid Atresia
5) Total Anomalous pulmonary venous return (TAPVR)
Tricuspid Atresia
characterized by absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability.
Left to right Shunts (late cyanosis)- Blue kids
VSD (most common congenital cardiac anomaly)
ASD
PDA
Eisenmenger’s syndrome
Uncorrected VSD, ASD or PDA causes compensatory pulmonary vascular hypertrophy which results in progressive pulmonary hypertension. As pulmonary resistance increases, the shunt reverses from left to right to right to left which causes late cyanosis, clubbing and polycythemia.
2q11 syndromes
truncus arteriosus, tetralogy of Fallot
Down Syndrome
ASD, VSD, AV septal defect (endocardial cushion defect)
Congenital Rubella
Septal defects, PDA, Pulmonary artery stenosis
Turner Syndrome
Coarctation of Aorta (preductal)
Marfan’s syndrome
aortic insufficiency and dissection (late complication)
Infant of diabetic mother
transposition of great vessels
atheromas
plaques in blood vessel walls
xanthomas
plaques or nodules composed of lipid-laden histiocytes in the skin, especially the eyelids (xanthelasma)
tendinous xanthoma
lipid deposit in tendon, especially achilles
Corneal arcus
lipid deposit in cornea, nonspecific (arcus senilis)
Arteriosclerosis- Monckeberg
Calcification in the media of the arteries, especially radial or ulnar. Usually benign; “pipestem”arteries. Does not obstruct blood flow.
Arteriolosclerosis
Two types: hyaline (thickening of small arteries in essential hypertension or diabetes mellitus) and hyperplastic (“onion skinning” in malignant hypertension)
Atherosclerosis
fibrous plaques and atheromas form in intima of arteries
Abdominal Aortic Aneurysm
associated with atherosclerosis. Occurs more frequently in hypertensive male smokers more than 50 years of age.
Thoracic aortic aneurysm
associated with hypertension, cystic medial necrosis (Marfan’s syndrome) and historically tertiary syphilis.
Coronary steal syndrome
vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to an area of higher perfusion
Symptoms of MI
diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, shortness of breath, fatigue.
Most common cardiomyopathy?
Dilated (congestive) cardiomyopathy
Dilated cardiomyopathy etiologies?
Chronic alcohol abuse, wet Beri Beri, Coxsackie B Virus myocarditis, chronic cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis and peripartum cardiomyopathy.
Dilated cardiomyopathy Findings?
S3, dilated heart on ultrasound, balloon appearance on chest x-ray
Dilated cardiomyopathy treatment?
Na restriction, ACE inhibitors, diuretics, digoxin, heart transplant
Hypertrophic Cardiomyopathy?
Hypertrophied interventricular septum is too close to mitral valve leaflet, leading to outflow obstruction. Cause of sudden death in young athletes.
Hypertrophic cardiomyopathy findings?
normal sized heart, S4, apical impulses, systolic murmur
Hypertrophic cardiomyopathy treatment?
beta blocker or non-dihydropyridine calcium channel blocker (verapamil)
Restrictive/ obliterative cardiomyopathy
major causes include sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children) and hemochromatosis
Loffler’s Syndrome
endomyocardial fibrosis with a prominent eosinophilic infiltrate
CHF
Occurs in patients with an inherited or acquired abnormality of cardiac structure or function which is characterized by a constellation of clinical symptoms (dyspnea, fatigue) and signs (edema, rales).
cause of cardiac dilation?
greater ventricular end-diastolic volume
cause of dyspnea on exertion?
failure of cardiac output to increase during exercise
Left Heart Failure
Pulmonary edema, paroxysmal nocturnal dyspnea
Orthopnea (shortness of breath when supine)
Right heart failure
hepatomegaly (nutmeg liver)
peripheral edema
jugular venous distention
Pulmonary edema
increased pulmonary venous pressure that leads to pulmonary venous distention and transudation of fluid. Presence of hemosiderin-laden macrophages (“heart failure” cells) in the lungs
Orthopnea
increased venous return in supine position exacerbates pulmonary vascular congestion
Hepatomegaly
increased central venous pressure leads to increased resistance to portal flow. Rarely, leads to “cardiac cirrhosis”
Peripheral edema
increased venous pressure which leads to fluid transudation
jugular venous distention
increased venous pressure
bacterial endocarditis symptoms
1) fever (most common)
2) Roth’s spots- round white spots on retina surrounded by hemorrhage
3) Osler’s nodes- tender raised lesions on finger or toe pads
4) new murmur
5) Janeway lesions- small, painless, erythematous lesions on palm or sole
6) anemia
7) splinter hemorrhages on nail bed
Acute bacterial endocarditis
S. Aureus (high virulence). Large vegetations on previously normal valves. Rapid onset.
Subacute endocarditis
viridans streptococci (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. More insidious onset.
Acute pericarditis
commonly presents with sharp pain, aggravated by inspiration and relieved by sitting up and leaning forward. Presents with friction rub. Widespread ST-segment elevation and/or depression.
fibrinous acute pericarditis
caused by Dressler’s syndrome, uremia, radiation. Presents with loud friction rub.
serous acute pericarditis
viral pericarditis (often resolves spontaneously); noninfectious inflammatory diseases (rheumatoid arthritis, SLE)
Suppurative/purulent acute pericarditis
usually caused by bacterial infections (pneumococcus, streptococcus). Rare now with antibiotics.
Cardiac tamponade
compression of heart by fluid in pericardium, leading to decreased CO. Equilibration of diastolic pressures in all 4 chambers. Findings: hypotension, increased venous pressure, distant heart sounds, increased heart rate, pulsus parodoxus
Pulsus parodoxus
decrease in amplitude of systolic blood pressure by more than 10 mm Hg during inspiration. Seen in severe cardiac tamponade, asthma, obstructive sleep apnea, pericarditis and croup.
Myxomas
most common primary cardiac tumor in adults. Usually described as a ball valve obstruction in the left atrium (associated with multiple syncopal episodes).
Rheumatic Fever
1) Fever
2) Erythema marginatum
3) Valvular damage (vegetation and fibrosis)
4) ESR increase
5) Red hot joints (migratory polyarthritis)
6) Subcutaneous nodules
7) St. Vitus’ dance (Sydenham’s chorea)
Acute Pericarditis
presents with sharp pain, aggravated by inspiration and relieved by sitting up and leaning forward. Presents with friction rub. ECG changes include widespread ST-segment elevation and/or PR depression.
3 Types: fibrinous, serous, suppurative/purulent
Fibrinous Acute pericarditis
caused by Dressler’s syndrome, uremia, radiation. Presents with loud friction rub.
Serous Acute pericarditis
Viral pericarditis (often resolves spontaneously), noninfectious inflammatory diseases (rheumatoid arthritis, SLE)
Cardiac Tamponade
compression of heart by fluid (blood, effusions) in pericardium, leading to decreased CO. Equilibration of diastolic pressures in all 4 chambers.
Findings: hypotension, increased venous pressure, distant heart sounds, increased heart rate, pulsus paradoxus.
Syphilitic heart disease
tertiary syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of the vessel wall and dilation of the aorta and valve ring. May see calcification of the aortic root and ascending aortic arch. Leads to tree bark appearance of the aorta. Can result in aneurysm of the ascending aorta or aortic arch and aortic insufficiency.
Rhabdomyomas
most frequent primary cardiac tumor in children (associated with tuberous sclerosis)
suppurative/purulent acute pericarditis
usually caused by bacterial infections (pneumococcus, streptococcus). Rare now with antibiotics.
Kussmaul’s sign
increase in JVP on inspiration instead of a normal decrease. May be seen with constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors, or cardiac tamponade.
Raynaud’s phenomenon
decreased blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress. Most often in the fingers and toes.
Temporal (giant cell) arteritis epidemiology
generally elderly females, unilateral headache (temporal artery), jaw claudication. May lead to irreversible blindness due to ophthalmic artery occlusion. Associated with polymyalgia rheumatica.
Temporal (giant cell) arteritis pathology
most commonly affects branches of carotid artery, focal granulomatous inflammation, increased ESR, treat with high dose corticosteroids.
Takayasu’s arteritis epidemiology
asian females less than 40 years of age, “pulseless disease” (weak upper extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances.
Takayasu’s arteritis pathology
granulomatous thickening of aortic arch, proximal great vessels, increased ESR, treat with corticosteroids.
Large vessel vasculitis
1) temporal (giant cell) arteritis
2) takayasu’s arteritis
medium vessel vasculitis
1) polyarteritis nodosa
2) kawasaki disease
3) Buerger’s disease (thromboangiitis obliterans)
Polyarteritis nodosa epidemiology
young adults, hepatitis B seropositivity in 30% of patients. Fever, weight loss, malaise, headache. GI: abdominal pain, melena. Hypertension, neurologic dysfunction, cutaneous eruptions, renal damage.
Polyarteritis nodosa pathology
Typically involves renal and visceral vessels, not pulmonary arteries. Immune complex mediated. Transmural inflammation of the arterial wall with fibrinoid necrosis. Lesions are of different ages. Many aneurysms and constrictions on arteriogram. Treat with corticosteroids, cyclophosphamide.
Kawasaki disese epidemiology
Asian children less than 4 years of age. Fever, cervical lymphadenitis, conjunctival injection, changes in lips/oral mucosa (strawberry tongue), hand foot erythema and desquamating rash.
Kawasaki disease pathology
may develop coronary aneurysms. Treat with IV immunoglobulin and aspirin.
Buerger’s disease (thromboangitis obliterans) epidemiology
heavy smokers, males less than 40 years of age. Intermittent claudication may lead to gangrene, autoamputation of digits, superficial nodular phlebitis. Raynaud’s phenomenon is often present.
Buerger’s disease pathology
segmental thrombosing vasculitis, treat with smoking cessation.
small vessel vasculitis
1) microscopic polyangitis
2) wegener’s granulomatosis (granulomatosis with polyangitis)
3) Churg-Strauss syndrome
4) Henoch-Schonlein purpura
Microscopic polyangitis epidemiology
necrotizing vasculitis commonly involving lung, kidneys and skin with pauci-immune glomerulonephritis and palpable purpura
Microscopic polyangitis pathology
no granulomas, p-ANCA, treat with cyclophosphamide and corticosteroids
Wegener’s granulomatosis epidemiology
upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis.
Lower respiratory tract: hemoptysis, cough, dyspnea.
Renal: hematuria, red cell casts
Wegener’s granulomatosis pathology
Triad:
1) focal necrotizing vasculitis
2) necrotizing granulomas in the lung and upper airway
3) necrotizing glomerulonephritis
c-ANCA, treat with cyclophosphamide, corticosteroids.
chest x-ray: large nodular densities
Churg-Strauss Syndrome epidemiology
asthma, sinusitis, palpable purpura, peripheral neuropathy (wrist/foot drop). Can also involve heart, GI, kidneys (pauci-immune glomerulonephritis)
Churg-Strauss Syndrome pathology
granulomatous, necrotizing vasculitis with eosinophilia. p-ANCA, elevated IgE level.
Henoch-Schonlein purpura epidemiology
most common childhood systemic vasculitis. Often follows URI. Classic triad:
1) skin: palpable purpura on buttocks/legs
2) Arthralgia
3) GI: abdominal pain, melena, multiple lesions of same age.
Henoch-Schonlein purpura pathology
vasculitis secondary to IgA complex deposition. Associated with IgA nephropathy.
Strawberry Hemangioma
benign capillary hemangioma of infancy. appears in first weeks of life; grows rapidly and regresses spontaneously at 5-8 years of age.
Cherry Hemangioma
Benign capillary hemangioma of the elderly. Does not regress. Frequency increases with age.
Pyogenic Granuloma
Polypoid capillary hemangioma that can ulcerate and bleed. Associated with trauma and pregnancy.
Cystic Hygroma
Cavernous Lymphangioma of the neck. Associated with turner syndrome.
Glomus Tumor
benign, painful, red-blue tumor under fingernails. Arises from modified smooth muscle cells of glomus body.
Bacillary Angiomatosis
benign capillary skin papules found in AIDS patients. Caused by Bartonella Henselae infections. Frequently mistaken for Kaposi’s sarcoma.
Angiosarcoma
Rare blood vessel malignancy typically occurring in the head, neck and breast areas. Associated with patients receiving radiation therapy, especially for Breast cancer and Hodgkin’s lymphoma. Very aggressive and difficult to resect due to delay in diagnosis.
Lymphangiosarcoma
lymphatic malignancy associated with persistent lymphedema (post-radical mastectomy).
Kaposi’s sarcoma
endothelial malignancy most commonly of the skin, but also mouth, GI tract and respiratory tract. Associated with HHV-8 and HIV. Frequently mistaken for bacillary angiomatosis.
Sturge-Weber Disease
congenital vascular disorder that affects capillary sized blood vessels. Manisfests with port-wine stain (nevus flammeus) on face, ipsilateral leptomeningeal angiomatosis (intracerebral AVM), seizures, and early onset glaucoma. Affects small vessels.
essential hypertension therapy
diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers.
CHF therapy
diuretics, ACE inhibitors/ARBs, beta blockers (compensated CHF), K sparing diuretics.
Diabetes Mellitus therapy
ACE inhibitors/ARBs, calcium channel blockers, diuretics, beta blockers, alpha blockers.
calcium channel blockers
nifedipine, verapamil, diltiazem, amlodipine
clinical use of calcium channel blockers
hypertension, angina, arrhythmias (not nifedipine), Prinzmetal’s angina, Raynaud’s.
Toxicity of calcium channel blockers
cardiac depression, AV block, peripheral edema, flushing, dizziness and constipation.
Hydralazine Clinical use
severe hypertension, CHF, first line therapy for hypertension in therapy, with methyldopa. Frequently co-administered with a beta blocker to prevent reflex tachycardia.
Hydralazine toxicity
compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina, Lupus-like syndrome.
Malignant hypertension treatment
commonly used drugs include nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.
nitroprusside
short acting: increased cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide).
Fenoldopam
dopamine D1 receptor agonist: coronary, peripheral, renal, and splanchnic vasodilation. Decreased BP and increased natriuresis.
