Step 1 - CV 2

denniskwinn's version from 2015-04-25 15:58


Question Answer
R to L shunts1.Tetralogy of Fallot (most common cause of early cyanosis) 2. Transposition of grcat vessels 3. Truncus arteriosus 4. Tricuspid atresia 5. Total anomalous pulmonary venous return (TAPVR)
Persistent truncus arteriosusfailure of truncus arteriosus to divide into pulmonary trunk and aorta.
Tricuspid atresiacharacterized by absence of trIcuspid valve and hypoplastic right ventricle. -Requires both ASD and VSD for viability.
TAPVR pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc.)
L to R shuntsVSD (most common congenital cardiac anomaly), ASD (loud S1, wide, fixed split S2), PDA (close with indomethacin)
LtoR shunt frequencyVSD>ASD>PDA
VSD associationsCorrecte transposition, tetralogy, cri du chat, fetal alcohol
ASD associationsfetal alcohol, down syndrome, paradoxic embolus
PDA associationsCongenital rubella, Resp distress syndrome, Complete transposition
Eisenmenger’s syndromeUncorrected VSD, ASD , or PDA causes compensatory vascular hypertrophy, which results in progressive pulmonary hypertensIon. As pulmonary resistance ↑, the shunt reverses from L to R to R to L, which causes late cyanosis (clubbing and polycythemia)
Tetralogy of FallotPulm sten (most important for prognosis) , RVH, Overriding aorta (overVSD), VSD, Early cyanosIs caused by a R-to-L shunt across the VSD - b/c of ↑ pressure caused by stenotIc pulmonic valve. x-ray = boot-shaped heart due to RVH . "Tet (hypoxic) spells" - squatting increases systemic vasc resistance (compress femoral) = temporary reversal of shunt forcing unox blood into pulm artery.
Transposition of great vesselsAorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior) →separation of systemic and pulmonary circulations. shunt needed to allow adequate mixing of blood 2. Due to failure of aorticopulmonary septum to spiral - without surgery death in first months of life
Infantile coarctationaortic stenosis proximal to insertion of ductus arteriosus (preductal). - associated with turner’s syndrome
Adult coarctationstenosis is distal to ductus arteriosus (postductal). Associated with notching of the rib (due to collateral circulation), hypertension in upper extremities, weak pulses in lower extremities - also associated with bicuspid aortic valve
How to end PDA Indomethacin
How to maintain PDAPGE synthesis and low O2 tension
22q11 syndromes associationsTruncus arteriosus, tetralogy of Fallot
Down syndrome associationsASD, VSD, AV septal defect (endocardial cushion defect)
Congenital rubella associationsSeptal defects, PDA, Pulm artery stenosis
Turner's syndrome associationsCoarctation of Aorta
Marfan's syndromc associationsAortic insufficiency (late complication)
Infant of diabetic mother associationsTransposition of great vessels


Question Answer
Hypertension risk factors↑age, obesity, diabetes, smoking, genetics, Black>white>asian
HTN definitionBP > 140/90
BP features90% is primary (essential) and related to ↑ CO or ↑ TPR; remaining 10% mostly secondary to renal disease.
HTN predisposes toAtherosclerosis, left ventricular hypertrophy, stroke, CHF, renal failure, retinopathy, and aortic dissection
AtheromasPlagues in blood vessel walls. - sign of hyperlipidemia
XanthomasPlagues or nodules composed of lipid-laden histiocytes in the skin, especially the eyelids (xanthelasma). - sign of hyperlipidemia
Tendinous xanthomaLipid deposit in tendon, especially Achilles. - sign of hyperlipidemia
Corneal arcusLipid deposit in cornea, nonspecific (arcus senilis). - sign of hyperlipidemia
Monckeberg Calcification in the media of the arteries, especially radial or ulnar. Usually benign; "pipestem" arteries. Does not obstruct blood flow; intima not involved.
Arteriolosclerosis Hyaline thickening of small arteries in essential hypertension or diabetes mellitus. - Hyperplastic "onion skinning" in malignant hypertension.
Atherosclerosis Fibrous plaques and atheromas form in intima of arteries
Aortic dissectionLongitudinal intraluminal tear forming a false lumen. Associated with hypertension or cystic medial necrosis Is (component of Marfan's syndrome). Presents with tearing chest pain radiating to the back. CXR shows mediastinal widening. The false lumen occupies most of the descending aorta. Can result In aortic rupture and death.
Atherosclerosis risk factorsSmoking, hypertension, diabetes mellitus, hyperlipidemia, family history.
Atherosclerosis progressionEndothelial cell dysfunction →macrophage and LDL accumulation → foam cell formation → fatty streaks ~ smooth muscle cell migration (involves PDCF and TGF-Beta ) → fibrous plaque → complex atheromas
Atherosclerosis complicationsAneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli .
Atherosclerosis locationAbdominal aorta> coronary artery> popliteal artery> carotid artery.
Atherosclerosis symptomsAngina, claudication, but can be asymptomatic
Manifestations of ischemic heart diseaseAngina, MI, Sudden cardiac death, Chronic ischemic heart disease
Angina definitionCAD narrowing >75%
Stable anginamostly secondary to atherosclerosis; ST depression on ECG (retrosternal chest pain with exertion)
Prinzmetal's anginaoccurs at rest secondary to coronary artery spasm; ST elevation on ECG
Unstable/crescendo anginathrombosis but no necrosis; ST depression on ECG (worsening chest pain at rest or with minimal exertion)


Question Answer
MI Symptomsdiaphoresis, nausea, vomiting, severe retrostemal pain, pain in left arm and/or jaw, SOB, fatigue, adrenergic symptoms
MI diagnosisIn the first 6 hours, ECG is the gold standard.changes can include ST elevation (transmural infarct), ST depression (subendocardial infarct), and pathologic Q waves (transmural infarct). 2. Cardiac troponin I rises after 4 hours and is elevated for 7- 10 days; more specific than other protein markers. 3. CK-MB is predominantly found In myocardium but can also be released from skeletal muscle. 4. AST is nonspecific and can be found in cardiac, liver, and skeletal muscle cells.
Characteristics of transmural infarcts↑ necrosis, affects entier wall, ST elevation on ECG
Characteristics of subendocardial infarctsDue to ischemic necrosis of (<50% of ventricle wall), Subendocardium especially vulnerable to ischemia, Due to fewer collaterals, higher pressure, ST depression on ECG
MI complications1. Cardiac arrhythmia-important cause of death before reaching hospital; common in first few days 2. LV failure and pulmonary edema 3. Cardiogenic shock (large Infarct- high risk of mortality) 4. Ventricular free wall rupture→cardiac tamponade; papillary muscle→severe mitral regurgitation; and interventricular septal rupture→VSD 5. Aneurysm formation - ↓CO, risk of arrhythmia, embolus from mural thrombus 6. Postinfarction fibrinous pericarditis- friction rub (3- 5 days post-MI) 7. Dressler's syndrome- autoimmune phenomenon resulting In fibrinous pericarditis (several weeks post-MI)
Causes of congestive cardiomyopathyAlcohol abuse, wet Benberi, Coxsackie B VIruS myocarditis, chronic Cocaine u e, Chagas' discase, Doxorubicin toxicIty, hemochromatosIs, and postpartum - ABCCCDHP
Congestive cardiomyopathysystolic dysfunction - eccentric hypertrophy - most common - S3, dilated heart on ultrasound, balloon appearance on chest x-ray
Hypertrophic cardiomyopathy HypertTophied IV septum is "too close" to mitral valve leaflet, leading to outflow tract obstruction and diastolic dysfunction . 50% of cases are familial, autosomal dominant. Associated with Friedreich's ataxia. Disoriented, tangled, hypertrophied myocardial fibers. Cause of sudden death in young athletes.
Hypertrophic cardiomyopathy findingsnormal-sized heart, S4, apical impulses, systolic murmur. Treat with P-blocker or non-dihydropyridine calcium channel blocker (e.g., verapamil )
Restrictive/obliterative cardiomyopathy causessarcoidosis, amyloidosIs, postradiation fibrosis, endocardial fibroelastosis, (thick fibroelastic tissue In endocardium of young children), Loffler's syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate), and hemochromatosis (dilated cardiomyopathy) can also occur - A HELPS - amyloid, hemochromatosis, endocardial fibroelas, Lofflers, Postradiation, Sarcoid
CHFA clinical syndrome that occurs In patients with an inherited or acquired abnormality of cardiac structure or function, who develop a constellation of clinical
CHF Symptoms: (dyspnea, fatigue) and signs (edema, rales).
Cause of Dyspnea on exertion in CHFFailure of LV output to ↑ during exercise
Cause of cardiac dilation in CHFGreater ventricular end diastolic volume
Cause of Pulmonary edema, Paroxysmal nocturnal dyspnea in CHFPulmonary venous distention and transudation of fluid. Presence of hemosiderin-laden macrophages in the lungs due to microhemorrhages from ↑ pulmonary capillary pressure.
Cause of Orthopnea in CHF↑ venous return in supine position exacerbates pulmonary vascular congestion .
Cause of Hepatomegaly (nutmeg liver) in CHF↑ central venous pressure→↑ resistance to portal flow. Rarely leads to “cardiac cirrhosis”
Cause of ankle, sacral edema in CHFRV failure→↑ venous pressure → fluid transudation
Cause of Jugular venous distention in CHFRight heart failure→↑ venous pressure


Question Answer
Bacterial endocarditis symptomsFROM JANE - Fever, Roth's spots, Osler's nodes, Murmur, Janeway lesions, Anemia, Nail-bed hemorrhage, Emboli
Bacterial endocarditis compilcationschordae rupture, glomerulonephritis, suppurative pericarditis, emboli
Tricuspid endocarditis associationIV drug abuse - S.Aureus, Pseudomonas, Candida (don’t tri drugs)
Roth 's spots(round white spots on retina surrounded by hemorrhage),
Osler's nodes (tender raised lesions on finger or toe pads)
Janeway lesions (small erythematous lesions on palm or sole)
Acute endocarditis S. aureus (high virulence). Large vegetations on previously normal valves, Rapid onset.
Subacute endocarditisviridans streptococci (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. - Sequela of dental procedures. More insidious onset.
Nonbacterial endocarditissecondary to malignancy or hypercoagulable state (marantic/thrombotic endocarditis) - s.bovic present in colon cancer, S.epidermidis on prosthetic valves. HACEK organisms cause culture-negative endocarditis
Libman-Sacks endocarditisVerrucous (wartlike), sterile vegetations occur on both sides of the valve. Most often benign; can be associated with mitral regurgitation and, less commonly, mitral stenosIs. The most common heart manifestation of SLE is in fact pericarditis
Rheumatic heart disease symptomsFever, Erythema marginatum, Valvular damage (vegetation And fibrosis), ESR ↑, Red-hot joints (migratory polyarthritis), Subcutaneous nodules, St. Vitus dance (chorea) - FEVERSS
Rheumatic heart diseasefrom pharyngeal infection with GAS -(type II sensitivity- abs vs M proteins) Early death=myocarditis, Late sequelae= rheumatic heart disease→ heart valves - mitral > aortic>> tricuspid (high-pressure valves most) Early lesion is MVP; late lesion is mitral stenosis. Associated with Aschoff bodies (granuloma with giant cells). Anitschkow’s cells (activated histiocytes), elevated ASO titers.
RFever treatmentpenicillin, aspirin, corticosteroids if murmur, chronic penicillin to prevent recurrence
Cardiac tamponadeCompression of heart by fluid (e.g., blood, effusions) in pericardium, leading to ↓ CO - Equilibration of diastolic pressures in all 4 chambers.
Tamponade findingshypotension, ↑ venous pressure (JVD), distant heart sounds, ↑ HR, pulsus paradoxus.
Pulsus paradoxusexaggerated ↓ in amplitude of pulse during inspiration Seen In severe cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, and croup.\
Serous pericarditisCaused by SLE, rheumatoid arthritis, viral Infection, uremia.
Fibrinous pericarditisUremIa, Ml (Dressler's syndrome), rheumatic fever.
Hemorrhagic pericarditisTB, Malignancy (e.g., melanoma).
Pericardial Findingspericardial pain, friction rub, pulsus paradoxus, distant heart sounds. ECG changes with ST- segment elevation in multiple leads
Pericarditis outcomeCan resolve without scarring or lead to chronic adhesive or chronic constrictive pericarditis.
Syphilitic heart diseasetertiary Syphilis disrupts the vasa vasorum of the aorta with consequent dilation of the aorta valve ring. may see caicification 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 valve incompetence
Myxomamost common primary cardiac tumor in adults. 90% occur in the atria (mostly left atrium). myxomas are usually described as a "ball-valve" - obstruction In the left atrium (associated with multiple syncopal episodes).
Rhabdomyomasmost Frequent primary cardiac tumor in children (associated with tuberous sclerosis).
Metastases most common heart tumor (melanoma, lymphoma).
Kussmaul's sign ↑ in jugular venous pressure on inspiration.


Question Answer
TelangiectasiaArteriovenous malformation in small vessels - dilated vessels on skin and mucous membranes - affects small vessels
Hereditary hemorrhagic telangiectasia (0sler Weber-Rendu syndrome) - autosomal-dominant inheritance. Presents with recurrent epistaxis, skin discolorations, mucosal telangiectasias, and GI bleeds.
Varicose veinsDilated, tortuous superficial veins due to chronically ↑ venous pressure. Predisposes to poor wound healing and varicose ulcers - rarely causes thromboembolism
Raynauds disease↓ blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress . Most often in the fingers and toes called phenomenon (not disease) when secondary to a mixed connectlve ttssue disease, (SLE, CREST)