Flashcards in Cardiovascular Disease Deck (133):
Embryonic structure that gives rise to ascending aorta and pulmonary trunk
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
Starts at week 4 and establishes the right-left polarity.
Seen in Kartagener as left-right dynein is required for proper cardiac looping
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
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
Yolk sac from week 3-8
Liver from 6 weeks to birth
Spleen from 10-28 weeks
Bone marrow from 18 weeks to adult
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
Shunts blood entering the fetus through the umbilical vein to the IVC to bypass hepatic circulation
Shunts oxygenated blood entering the RA from the IVC to LA to bypass the pulmonary circulation
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
Adult derivative of ductus venosus
Adult derivative of foramen ovale
Adult derivative of notochord
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=CO x TPR
MAP=2/3 diastolic pressure + 1/3 systolic pressure
Stroke volume formula
SV = EDV - ESV
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
EF = SV/EDV
Decreased in systolic HF; normal in diastolic HF
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.
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
Inspiration causes decreased intrathoracic pressure, increasing venous return and increasing RV ejection time and delaying closure of pulmonic valve.
Seen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block)
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.
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.
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
AD disorder. Pseudo-right bundle branch block and ST elevations in V1-V3 on ECG. Risk of ventricular tachyarrhythmias and SCD. Treated with ICD.
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.
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
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)
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
Asymptomatic at birth; can manifest weeks later or remain asymptomatic. USually self-resolve. Causes holosystolic blowing murmur.
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
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
Renal arterial hyalinosis on PAS
Plaques or nodules of lipid-laden histiocytes in skin, especially seen on the eyelids
Lipid deposits in tendons, especially seen in Achilles tendon
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.
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
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
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
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
-coxsackie B virus
-chronic cocaine use
Also: hemochromatosis, sarcoidosis, peripartum cardiomyopathy
Clinical findings of dilated cardiomyopathy
Heart failure, S3, systoic regurg murmur, balloon appearance of heart on CXR
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
round white spots on retina surrounded by hemorrhage; associated with endocarditis
tender raised lesions on finger or toe pads; associated with endocarditis
small painless erythemtaous lesions on palm or sole; associated with endocarditis
Rheumatic fever presentation
-joint involvement: migratory polyarthritis
-nodules in skin - subcutaneous
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
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
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.
Benign capillary skin papules seen in AIDS patients due to Bartonella henselae infections
Benign capillary hemangioma seen in elderly. Does not regress
Cavernous lymphangioma of neck. Seen in turner syndrome
Benign, painful, red-blue tumor under fingernails
Endothelial malignancy associated with HHV-8 and HIV. Lymphocytic infiltrate (distinguishes from bacillary angiomatosis which has neutrophilic infiltrate)
Polypoid capillary hemangioma. Associated with trauma dn pregnancy. Can ulcerate and bleed
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
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
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
Seen in asian kids
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.
Necrotizing vasculitis of lungs, kidneys, skin. Pauci-immune glomerulonephritis. Palpable purpora. No nasopharyngeal involvement
Also called eosinophilic granulomatosis with polyangiits. Causes asthma, sinusitis, skin nodules, purpora, peripheral nueropathy.
Granulomatous, necrotizing vasculitis
p-ANCA pos with increased IgE
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