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Flashcards in Cardiovascular Disease Deck (133):

Truncus arteriosus

Embryonic structure that gives rise to ascending aorta and pulmonary trunk


Bulbus cordis

Embryonic structure that gives rise to outflow tract of R and L ventricles


Primitive atrium and primitive ventricle

Give rise to trabeculated portions of atria and ventricles


Primitive pulmonary vein

Gives rise to smooth part of left atrium


Left and right horns of sinus venosus

Left gives rise to coronary sinus
Right gives rise to smooth part of right atrium


Embryonic structures that give rise to SVC

Right common cardinal vein and right anterior cardinal vein


Cardiac looping

Starts at week 4 and establishes the right-left polarity.



Seen in Kartagener as left-right dynein is required for proper cardiac looping


Atrial septation

1. Septum primum grows
2. Foramen secundum forms in septum primum
3. Septum secundum forms; foramen secundum maintains R to L shunt
4. Septum secundum expands leaving just small opening, the foramen ovale
5. Septum primum and secundum fuse to form atrial septum
6. Increased LA pressure closes foramen ovale after birth


Ventricular septation

1. Muscular ventricular septum forms with interventricular foramen as an opening
2. Formation of membranous interventricular septum
3. Endocardial cushions grow to separate atria from ventricles. Contribute to atrial septation as well as the membranous portion of the interventricular septum


Fetal erythropoiesis

Yolk sac from week 3-8
Liver from 6 weeks to birth
Spleen from 10-28 weeks
Bone marrow from 18 weeks to adult


Fetal hemoglobin

Higher O2 affinity due to less 2,3 BPG binding


Fetal circulation: umbilical vein and artery

Umbilical vein brings blood from placenta to fetus. High O2 saturation

Umbilical arteries bring blood from fetus back to placenta. Low O2 saturation


Ductus venosus

Shunts blood entering the fetus through the umbilical vein to the IVC to bypass hepatic circulation


Foramen ovale

Shunts oxygenated blood entering the RA from the IVC to LA to bypass the pulmonary circulation


Ductus arteriosus

Shunts deoxygenated blood entering the RA and then RV from the SVC from the pulmonary artery to the descending aorta. Occurs due to high fetal pumonary artery resistance which is due to the low O2 tension.


Changes in circulation at birth

Infant takes a breath which causes decreased resistance in the pulmonary vasculature, allowing blood to flow through and increasing LA pressure relative to RA pressure. This causes foramen ovale to close.

Increase in O2 and decrease in PG related to placental separation results in closure of the ductus arteriosus


Adult derivative of allantois/urachus

median umbilical ligament


Adult derivative of ductus arteriosus

ligamentum arteriosum


Adult derivative of ductus venosus

Ligamentum venosum


Adult derivative of foramen ovale

Fossa ovalis


Adult derivative of notochord

Nucleus pulposus


Adult derivative of umbilical arteries

medial umbilical ligaments


adult derivative of umbilical vein

ligamentum teres which is within the falciform ligament


Blood supply to SA and AV nodes

Right coronary artery. Block can cause bradycardia or heart block


Right vs left dominant circulation

Right dominant seen in 85%. PDA arises from the RCA.

Left dominant seen in 8%. PDA arises from LCX

Codominant circulation in 7%. PDA arises from both RCA and LCX


Left atrium anatomy

Most posterior portion of the heart. Enlargement can cause dysphagia or hoarseness


Mean arterial pressure ormula


MAP=2/3 diastolic pressure + 1/3 systolic pressure


Stroke volume formula



Cardiac output during exercise

During early stages, CO maintained by increased HR and increased SV. During late stages, maintained by increased HR only as SV plateaus, Diastole preferentially shortened when HR increases resulting in decreased filling time and decreased CO


Causes of increased and decreased pulse pressure

Increased: hyperthyroidism, aortic regurg, aortic stiffening, OSA, exercise

Decreased: aortic stenosis, cardiogenic shock, cardiac tamponade, advanced HF


Effect of decreased sodium on heart

Decreased extracellular sodium results in decreased activity of the Na+/Ca++ exchanger, decreasing contractility


Effect of digitalis on heart

Blocks Na+/K+ pump, increasing intracellular Na+ and increasing intracellular Ca++ via decreased Na+/Ca++ exchanger activity


Formula for wall tension

Wall tension = (pressure x radium) / (2 x wall thickness)


Preload and afterload

Preload approximated by EDV. Depends on venous tone and circulating blood volume. Decreased by venodilators like nitroglycerin

Afterload approximated by MAP. Hypertrophies to compensate for increased afterolad. Decreased with vasodilators like hydralazine.

ACEs and ARBs decrease both preload and afterload


Ejection fraction


Decreased in systolic HF; normal in diastolic HF


Starling curve

Shows that stroke volume increases with ventricular EDV. Corresponds with the optimal sarcomere length that can generate tension.


Changes in exercise

Increase in inotropy and decreased TPR to maximize CO.


Heart sounds

S1: Mitral and tricuspid valve closure
S2: Aortic and pulmonary valve closure
S3: Heard in early diastole during rapid filling phase. Heard when there are increased filling pressures of dilated ventricles
S4: Heard in late diastole. Heard when there is high atrial pressure such as in ventricular hypertrophy due to LA pushing against a stiff LV wall


Jugular venous pulse (JVP)

a wave: atrical contraction
c wave: RV contraction
x descent: atrial relaxation
v wave: increased RA pressure due to filling
y descent: RA emptying into RV


Physiologic splitting

Inspiration causes decreased intrathoracic pressure, increasing venous return and increasing RV ejection time and delaying closure of pulmonic valve.


Wide splitting

Seen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block)


Fixed splitting

Seen in ASD due to left to right shunt that increases RA and RV volumes, increasing flow through pulmonic valve so that pulmonic closure is always delayed.


Paradoxical splitting

Seen when aortic valve closure delayed. A2 is delayed and heard after P2. During inspiration, P2 delayed, moves closer to A2, eliminating the split


Effect of inspiration on heart sounds

Increases venous return to RA increasing intensity of right heart sounds


Effect of hand gripping on heart sounds

Increases afterload, increasing intensity of MR, AR, and VSD murumurs but decreasing hypertrophic cardiomyopathy murmurs. Delays click of MVP.


Valsalva maneuvers

Decreases preload by increasing intrathoracic pressure. Decreases intensity of most murmurs, but increases intensity of hypertrophic cardiomyopathy murmur and causes earlier click of MVP.


Rapid squatting: effect on heart sounds

Increases venous return causing increased intensity of AS murmur, decreased intensity of hypertrophic cardiomyopathy murmur


Mitral valve prolapse murmur

Late systolic crescendo murmur with midsystolic click. Valsalva maneuver or standing decreases LV volume allowing prolapse to occur sooner and more severely


Myocardial action potential

Phase 0: Rapid upstroke and depolarization, VG Na+ channels open

Phase 1: Initial repolariztion due to inactivation of VG Na+ channels and opening of VG K+ channels

Phase 2: Plateau due to VG Ca++ influx balancing K+ efflux. Ca++ influx triggers Ca++ release from SR and myocyte contraction

Phase 3: Rapid replarization due to opening of VG slow K+ channels and closure of VG Ca++ channels

Phase 4: Resting potential with high K+ permeability



Pumps calcium back into the sarcoplasmic retirculum after cardiac contraction.


Pacemaker action potential

Phase 0: Upstroke due to opening of VG Ca++ channels. VG Na++ channels permanently inactivated because resting voltage less negative

Phase 3: Inactivation of VG Ca++ channels; opening of K+ channels and K+ efflux

Phase 4: Slow spontaneous depolarization due to funny current: both Na+ and K+ transduction. Slope determines HR


ECG: P wave, QRS, T wave, and U wave

P wave: atrial depolarization
QRS: ventricular depolarization (less than 120 ms)
T wave: ventricular repolarization
U wave: seen in hypokalemia and bradycardia


Torsades de pointes

Shifting sinusoidal waveforms. Caused by drugs that induce long QT (class IA and III antiarrhythmics, macrolides, haloperidol, TCADs, ondansetron). Treated wtih magnesium sulfate


Congenital long QT syndrome

Disorder of myocardial repolarization due to ion channel defects. Risk of sudden death due to torsades


Brugada syndrome

AD disorder. Pseudo-right bundle branch block and ST elevations in V1-V3 on ECG. Risk of ventricular tachyarrhythmias and SCD. Treated with ICD.


Wolff-Parkinson-White syndrome

Abnormally fast conduction from atria to ventricle that bypasses the AV node. Causes ventricles to depolarize early in part. On ECG see delta wave and widened QRS. Can cause reentry sircuit and supraventricular tachycardia


First degree heart block

Prolonged PR over 200msec. Benign and asymptomatic, does not require treatment.


Second degree heart block

Mobitz type I: progressive lengthening of PR until beat is dropped. Usually asymptomatic.

Mobitz type II: dropped beats not preceded by change in PR length. Can progress to 3rd degree block so often treated with pacemaker.


Third degree heart block

Complete heart block in which atria and ventricles beat independently. Atrial rate faster than ventricular rate. Treated with pacemaker. Lyme disease is a cause.


Carotid massage

Increases pressure on carotid sinus, increasing stretch and increasing afferent baroreceptor firing. Decreases HR



Peripheral receptors in carotid and aortic bodies stimulated by low Po2, high Pco2, and low pH

Central stimulated by changes in pH and PCo2, not O2.



Approximates LA pressure. Normal is less than 12.


Causes of right to left shunt

5 Ts: truncus arteriosus, transposition, tricuspid atresia, tetralogy of fallot, TAPVR


Tricuspid atresia

Absence of tricuspid valve and hypoplastic RV. Requires both ASD and VSD for viability.


Tetralogy of Fallot

1) pulmonary infundibular stenosis (outflow obstruction; most important determinant for prognosis)
2) RVH
3) overriding aorta
4) VSD: right to left flow due to pulmonary stenosis leads to early tet spells

Squatting increases SVR, decreasing R to L shunt and improving cyanosis


Total anomalous pulmonary venous return (TAPVR)

Pulmonary veins drain into right heart


VSD presentation

Asymptomatic at birth; can manifest weeks later or remain asymptomatic. USually self-resolve. Causes holosystolic blowing murmur.


ASD presentation

Loud S1 and wide fixed split S2 (RV overload delays pulmonic valve closure). Defect usually in ostium secundum. Ranges from asymptomatic to HF


Risks for PDA

Prematurity, birth at altitude, maternal rubella


Eisenmenger syndrome

Uncorrect L to R shunt increases pulmonary blood flow leading to remodeling of he vasculature and pulmonary arterial HTN with compensatory RVH. Leads to reverseal of the shunt


Coarctation of aorta

Aortic narrowing near insertion of ductus arteriosus. Causes HTN in upper extremities and weak pulse in lower extremities with brachial femoral delay. Collateral arteries can erode the ribs over time resulting in notched appearance on CXR


Cardiac defects associated with down syndrome

AV septal defect, VSD, ASD


Cardiac dfects associated with diabetic mother

Transposition of great vessels


Hypertensive nephropathy

Renal arterial hyalinosis on PAS



Plaques or nodules of lipid-laden histiocytes in skin, especially seen on the eyelids


Tendinous xanthoma

Lipid deposits in tendons, especially seen in Achilles tendon


Corneal arcus

Lipid deposit in cornea. Common in elderly but seen earlier if there is hypercholesterolemia



Common finding. Wall thickening and loss of elasticity in small arteries and arterioles. Can be hyaline in HTN or diabetes or hyperplastic (onion skinning) in severe HTN with proliferation of sm muscle


Medial calcific sclerosis

Uncommon finding. Arteriosclerosis in medium sized arteries with calcification of elastic lamina. Causes vascular stiffening without obstruction as the intima is not involved



Affects elastic arteries and large and med muscular arteries. Buildup of cholesterol plaques.

Endothelial dysfunction leads to macrophage and LDL accumulation. Macrophages eat the LDL to form foam cells. This results in fatty streaks and smooth muscle cell migration. ECM deposits forming a fibrous plaque.

Most common location is abdominal aorta followed by coronary artery and popliteal artery.


Aortic aneurysm

Localized dilatation of the aorta involving all three layers. Presents with abdominal or back pain when leaking, dissecting, about to rupture

AAA associated with atherosclerosis. Risk factors are smoking, age, male, family history.

Thoracic aortic aneurysm is associated with cystic medial degeneration. Risk factors are HTN, bicuspid aortic calce, and Marfan syndrome


Aortic dissection

Longitudinal intimal tear that forms a false lumen. Associated with HTN, bicuspid aortic valve, Marfan syndrome.

Presentation: tearing chest pain radiating to back, may have unequal BP in arms. Mediastinal widening on CXR.

Stanford type A: involves ascending aorta and is treated surgically

Stanford type B: involves descending aorta and or the arch. Treated with beta blockers and vasodilators.


Types of angina

Stable: atherosclerosis; ST depression during episodes

Variant: coronary artery spasm; transient ST elevation during episodes; triggered by tobacco, cocaine, triptans

Unstable: thrombosis with incomplete occlusion; may see ST depression and/or T wave inversion on ECG but no cardiac biomarker elevation. Increased frequency or intesnstiy of chest pain or chest pain at rest


Coronary steal syndrome

Basis of pharmacologic stress tests. Vessels distal to coronary stenosis are maximally dilated at baseline. When give a vasodilator, normal vessels dilate and blood is shunted toward well-perfused areas, decreasing flow and causing ischemia in the poststenotic region


Pathologic changes and complications seen in first 24 hours of MI

First 4 hours: No pathologic changes.

4-24 hours: Coagulative necrosis begins and neutrophils appear. Reperfusion injury can cause contraction bands (hypercontraction of sarcomeres due to massive Ca++ influx) via free radical damage to lipid membranes

Risk of arrhythmia, HF, cardiogenic shock


Pathologic changes and complications seen in first two weeks after MI

Days 1-3: Extensive coagulative necrosis and acute inflammation. Risk of postinfarctive fibrinous pericarditis

Days 3-14: Macrophages and granulation tissue. Risk of free wall rupture and tamponade or papillary muscle rupture and mitral regurg. Also risk of LV pseudoanerysm rupture


Pathologic changes and complications seen in months following MI

From 2wks to 3 mos after MI see contracted scar completion.

Risk of Dressler syndrome, HF, arrhythmia, true ventricular aneurysm rupture


MI diagnosis

ECG is gold standard in first 6 hors.

Troponin I rises after 4 hrs and remains elevated for 7-10 days

CK-MB rises aftet 6-12 hours and reutrns to normal after 48 hours. Less specific as can also be released from skeletal mscle


ECG localization of STEMI

V1-V2: anteroseptal infarct due to LAD occlusion
V3-V4: anteroapical infarct due to distal LAD occlusion
V5-V6: anterolateral infarct due to LAD or LCX occlusion
I, aVL: Lateral infarct due to LCX occlusion
II, III, aVF: inferior infarct due to RCA occlusion


Dressler syndrome

Autoimmune phenomenon resulting in fibrinous pericarditis several weeks post-MI. Friction rub soon after related to postinfarct fibrinous pericarditis


Pathophys of tetralogy of fallot

Abnormal neural crest cell migration leads to deviation of the infundibular septum during development resultaing in the misalignemnt of the aorta and the VSD



Caused by vitamin B1 deficiency.

Infantile beriberi: age2-3 mos. Cardiomegaly, tachycardia, cyanosis, dyspnea, vomiting

Adult dry beriberi: symmetric peripheral neuropathy with sensory and motor impairments

Adult wet beriberi: neuropathy + cardiomegaly, cardiomyopathy, CHF, peripheral edema, tachycardia


Great saphenous vein

Used for coronary bypasses. Runs from medial foot up medial leg and then inferolateral to pubic tubercle and anterior pubic rami before joining common femoral vein


Causes of dilated cardiomyopathy

Usually idiopathic of familial

Others: ABCCCD
-alcohol abuse
-wet beriberi
-coxsackie B virus
-chronic cocaine use
-chagas disease
-doxorubicin toxicity

Also: hemochromatosis, sarcoidosis, peripartum cardiomyopathy


Clinical findings of dilated cardiomyopathy

Heart failure, S3, systoic regurg murmur, balloon appearance of heart on CXR


Restrictive cardiomyopathy

Caused by infiltrative processes - sarcoidosis, amyloidosis, fibrosis, hemochromatosis

Diastolic dysfuction due to stiff noncompliant ventricles but normal systolic function.

Poor prognosis as little treatment is available


Systolic vs diastolic dysfunction in HF

Systolic: decreased EF, increased EDV, decreased contractility

Diastolic: preserved EF, normal EDV, decreased compliance, often due to myocardial hypertrophy.


Pathologic finding in lungs of heart failure patients

Hemosiderin laden macrophages: hemosiderin produced from breakdown of RBCs and is phagocytosed by macrophages


Preload, CO, and afterload in hypovolemic vs cardiogenic vs septic/anaphylactic shock

Hypovolemic: Cold and clammy skin. Decreased preload, decreased CO, increased afterload

Cardiogenic: Cold and clammy skin. Increased preload, decreased CO, increased afterload

Septic: Warm and dry skin. Decreased preload, increased CO, decreased afterload


Roth spots

round white spots on retina surrounded by hemorrhage; associated with endocarditis


Osler nodes

tender raised lesions on finger or toe pads; associated with endocarditis


Janeway lesions

small painless erythemtaous lesions on palm or sole; associated with endocarditis


Rheumatic fever presentation

JONES criteria
-joint involvement: migratory polyarthritis
-nodules in skin - subcutaneous
-erythema marginatum
-sygenham chorea


Aschoff bodies

noncaseating granulomas with multinucelated giant cells; pathogneumonic for rheumatic heart disease; contain Anitxchkow cells which are enlarged macrophages


Acute pericarditis: presenation and treatment

Presentation: sharp pain aggravated by inspiration, relieved by sitting up and leaving foroward. Friction fub. Widespread ST elevation and or PR depression on ECG

Treatment: NSAIDs, steroids


Cardiac tamponade

Compression of heart by fluid in pericardial space resulting in decreased CO.

Presentation: hypotension, JVD, distant heart sounds, increased HR, pulsus paradoxus (decreased in systolic BP greater than 10 during inspiration due to decreased RV filling

ECG: low voltage QRS and electrical alterans

Treatment: no diuresis as pressures need to be kept high


Syphilitic heart disease

Tertiary syphilis disrupts vasa vasorum of aorta causing atrophy of vessel wall and dilatation of aorta and valve ring. Can cuase calcification of aortic root and ascending aortic arch



Most common cardiac tumor in adults. Most often in LA which can disrupt the mitral valve and result in syncope.



Most common cardiac tumor in kids. Associated with tuberous sclerosis


Kussmaul sign

Increased JVP on inspiration (normall decreases). Seen iwth constrictive pericarditis, restrictive cardiomyopathy, tumors.

Due to negative intrathoracic pressure during breathing not being transmitted to the heart and impairing RV filling, resulting in back up of blood



BV tumor ousually on head, neck, breast. Seen in elderly. Associated with radiation therapy and postmastectomy-lymphedema.


Bacillary angiomatosis

Benign capillary skin papules seen in AIDS patients due to Bartonella henselae infections


Cherry hemangioma

Benign capillary hemangioma seen in elderly. Does not regress


Cystic hygroma

Cavernous lymphangioma of neck. Seen in turner syndrome


Glomus tumor

Benign, painful, red-blue tumor under fingernails


Kaposi sarcoma

Endothelial malignancy associated with HHV-8 and HIV. Lymphocytic infiltrate (distinguishes from bacillary angiomatosis which has neutrophilic infiltrate)


Pyogenic granuloma

Polypoid capillary hemangioma. Associated with trauma dn pregnancy. Can ulcerate and bleed


Strawberry hemangioma

Benign capillary hemangioma seen in first few weeks of life that grows rapidly and then regresses spontaneously


Treatment of Raynauds

Ca++ channel blocker


Derivatives of aortic arches

First: maxillary artery
Second: hyoid artery and stapedial artery
Third: common carotid and proximal internal carotid arteries
Fourth: aortic arch and proximal right subclavian artery
Sixth: proximal pumonary arteries, ductus arteriosus


Cardiac catheterization through common femoral artery

Ideally enter below the inguinal ligament. Puncture above the iguinal ligament increases risk of retroperitoneal hemorrhage, which can't be controlled with manual compression.



Rare malignant neoplasm of lymphatic channel endothelium. Can occur as complication of persistent lymphedema following radical mastectomy


Pathologic findings of temporal arteritis

Focal granulomatous inflammation


Takayasu arteritis

Affects large arteries. Asian females less than 40. Also called pulseless disease due to weak upper extremity pulses. Fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances

Granulomatous thickening and narrowing of aortic arch and proximal great vessels


Polyarteritis nodosa

Affects medium vessels of young adults. Associated with hepB. Fever, weight loss, malaise, headache. Abdominal pain and melena due to mesenteric ischemia. HTN, neuro dysfunction, renal damage.

Involves renal and visceral vessels with sparing of lungs. Immne complex mediated. Transmural inflammation of vessel walls with fibrinoid necrosis


Kawasaki disease

Seen in asian kids


Buerger disease

Seen in males less than 40 who are heavy smokers. Intermittent claudication leading to gangrene and autoamputation to digits. Raynaud phenomenon

Segmental thrombosing vascultits

Treatment is smoking cessation


Granulomatosis wih polyangiits

Wegner's. Perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis.

Hemoptysis, cough, dyspnea.

Hematuria, red cell casts

Focal necrotizing vasculitis with granulomas in lungs and upper airway and necrotiizing glomerulonephritis.

c-ANCA positive


Microscopic polyangiitis

Necrotizing vasculitis of lungs, kidneys, skin. Pauci-immune glomerulonephritis. Palpable purpora. No nasopharyngeal involvement



Churg strauss

Also called eosinophilic granulomatosis with polyangiits. Causes asthma, sinusitis, skin nodules, purpora, peripheral nueropathy.

Granulomatous, necrotizing vasculitis

p-ANCA pos with increased IgE


Henoch-Schonlein purpora

Most common childhood vasculitis. Often follows URI. Palpable purpor on legs and butt, arthralgias, abdominal pain.

Secondary to IgA immune complex deposits; associate diwth IgA nephropathy


path findings of Burger's disease (vascultitis)

segmental vasculitis extending into contiguous veins and nerves