Cardiovascular- pathology Flashcards
Congenital heart diseases
- RIGHT-TO-LEFT SHUNTS
Early cyanosis—“blue babies.”
5 Ts:
- Truncus arteriosus (1 vessel)
- Transposition (2 switched vessels)
- Tricuspid atresia (3 = Tri)
- Tetralogy of Fallot (4 = Tetra)
- TAPVR (5 letters in the name)
Congenital heart diseases
- 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.
Congenital heart diseases
- D-transposition of great vessels
Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior). Not compatible with life unless a shunt is present to allow mixing of blood.
Not compatible with life unless a shunt is present to allow mixing of blood
Congenital heart diseases
- Tricuspid atresia
Absence of tricuspid valve and hypoplastic RV;
requires both ASD and VSD for viability.
Congenital heart diseases
- Tetralogy of Fallot
Caused by anterosuperior displacement of the
infundibular septum.
PROVe:
- Pulmonary infundibular stenosis (most important determinant for prognosis)
- Right ventricular hypertrophy (RVH)— boot‑shaped heart on CXR A
- Overriding aorta
- VSD
Most common cause of early childhood cyanosis.
Congenital heart diseases
- Total anomalous pulmonary venous return
Pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc); associated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO.
Congenital heart diseases
- Ebstein anomaly
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.
Congenital heart diseases
- LEFT-TO-RIGHT SHUNTS
Ventricular septal defect
Atrial septal defect
Patent ductus arteriosus
*Acyanotic at presentation; cyanosis may occur
years later.
Congenital heart diseases
- Ventricular septal defect
Most common congenital cardiac defect.
Asymptomatic at birth, may manifest weeks
later or remain asymptomatic throughout life
Frequency: VSD > ASD > PDA.
Congenital heart diseases
- Atrial septal defect
wide, fixed split S2.
Ostium secundum defects most common and usually an isolated finding; ostium primum defects rarer and usually occur with other cardiac anomalies.
May lead to paradoxical emboli (systemic venous emboli use ASD to bypass lungs and become systemic arterial emboli).
Congenital heart diseases
- Patent ductus arteriosus
In fetal period, shunt is right to left (normal).
Associated with a continuous, “machine-like” murmur. Patency is maintained by PGE synthesis and low O2 tension.
can eventually result in late cyanosis in the lower extremities (differential cyanosis).
Congenital heart diseases
- Eisenmenger syndrome
Uncorrected left-to-right shunt, high 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.
Congenital heart diseases
- 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 and notched appearance on CXR
Congenital cardiac defect associations
- Alcohol exposure in utero (fetal alcohol syndrome)
- Congenital rubella
- Down syndrome
- Infant of diabetic mother
VSD, PDA, ASD, tetralogy of Fallot
PDA, pulmonary artery stenosis, septal defects
AV septal defect (endocardial cushion defect), VSD, ASD
Transposition of great vessels, VSD
Congenital cardiac defect associations
- Prenatal lithium exposure
- Turner syndrome
- Williams syndrome
- 22q11 syndromes
- Marfan syndrome
Ebstein anomaly
Bicuspid aortic valve, coarctation of aorta
Supravalvular aortic stenosis
Truncus arteriosus, tetralogy of Fallot
MVP, thoracic aortic aneurysm and dissection, aortic regurgitation
Hypertension
90% of hypertension is 1° (essential). Remaining 10% mostly 2° to renal/renovascular diseases such as fibromuscular dysplasia (characteristic “string of beads”
appearance of renal artery) and atherosclerotic renal artery stenosis or to 1° hyperaldosteronism.
Hypertensive urgency
Hypertensive emergency
severe (≥ 180/≥ 120 mm Hg) hypertension without acute end-organ damage.
severe hypertension with evidence of acute end-organ damage (eg, encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia).
Hyperlipidemia signs
Xanthomas
Tendinous xanthoma
Corneal arcus
Arteriolosclerosis
Affects small arteries and arterioles.
Two types:
- hyaline (thickening of vessel walls inessential hypertension or diabetes mellitus)
- hyperplastic (“onion skinning” in severe hypertension)
Mönckeberg sclerosis (medial calcific sclerosis)
Affects medium-sized arteries. Calcification of internal elastic lamina and media of arterie. “Pipestem” appearance on x-ray. Does not obstruct blood flow
Atherosclerosis
Disease of elastic arteries and large- and medium-sized muscular arteries; a form of arteriosclerosis caused by buildup of cholesterol plaques.
Atherosclerosis
- Location
Abdominal aorta > coronary artery > popliteal artery > carotid artery
Atherosclerosis
- Progression
- endothelial cell dysfunction
- macrophage and LDL accumulation
- foam cell formation
- fatty streaks
- smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular matrix deposition
fibrous plaque - complex atheromas
Aortic aneurysm
pathologic dilatation of the aorta. May cause abdominal and/or back pain, which is a sign of leaking, dissection, or imminent rupture.
Abdominal aortic aneurysm
Associated with atherosclerosis. Risk factors include history of tobacco use, age, male sex, family history.
May present as palpable pulsatile abdominal mass. Most often infrarenal (distal to origin of renal arteries)
Thoracic aortic aneurysm
Associated with cystic medial degeneration.
Risk factors include hypertension, bicuspid aortic valve, connective tissue disease. Also associated with 3° syphilis.
Aortic root dilatation may lead to aortic valve
regurgitation.
Traumatic aortic rupture
most commonly at aortic isthmus (proximal descending
aorta just distal to origin of left subclavian artery).
Aortic dissection
Longitudinal intimal tear forming a false lumen.
Associated with hypertension, bicuspid aortic valve, inherited connective tissue disorders.
Can present with tearing, sudden-onset chest pain radiating to the back +/− markedly unequal BP in arms. CXR shows mediastinal widening.
Aortic dissection Types
Stanford type A (proximal): involves Ascending aorta. May extend to aortic arch or descending aorta. May result in acute aortic regurgitation or cardiac tamponade. Treatment: surgery.
Stanford type B (distal): involves only descending aorta (Below ligamentum arteriosum). Treat medically with β-blockers, then vasodilators.
Ischemic heart disease manifestations
- Stable Angina
usually 2° to atherosclerosis (≥ 70% occlusion); exertional chest pain in classic distribution (usually with ST depression on ECG), resolving with rest or nitroglycerin.
Ischemic heart disease manifestations
- Vasospastic Angina
at rest 2° to coronary artery spasm; transient ST elevation on ECG. Smoking is a risk factor. Triggers include cocaine, alcohol, and triptans.
Treat with Ca2+ channel blockers, nitrates, and smoking cessation.
Ischemic heart disease manifestations
- Unstable Angina
Thrombosis with incomplete coronary artery occlusion; +/− ST depression and/or T-wave inversion on ECG but no cardiac biomarker elevation. any chest pain at rest.
Ischemic heart disease manifestations
- Coronary steal syndrome
Distal to coronary stenosis, vessels are maximally dilated at baseline.
Administration of vasodilators (eg, dipyridamole, regadenoson) dilates normal vessels blood is shunted toward well-perfused areas ischemia in myocardium perfused by stenosed vessels.
Ischemic heart disease manifestations
- Sudden cardiac death
Death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia.
Associated with CAD (70% of cases), cardiomyopathy, and hereditary ion channelopathies.
Ischemic heart disease manifestations
- Non–ST-segment elevation MI (NSTEMI)
- ST-segment elevation MI (STEMI)
Transmural infarcts, Full thickness of myocardial wall involved, ST elevation on ECG, Q waves.
Subendocardial infarcts, Subendocardium (inner 1⁄3) especially, vulnerable to ischemia, ST depression on ECG.
*Commonly occluded coronary arteries: LAD > RCA > circumflex
Evolution of myocardial infarction
Pag. 300
Diagnosis of myocardial infarction
In the first 6 hours, ECG is the gold standard. Cardiac troponin I rises after 4 hours (peaks at 24 hr) and is raised for 7–10 days.
CK-MB rises after 6–12 hours (peaks at 16–24 hr), can also be released from skeletal muscle. Useful in diagnosing reinfarction following acute MI because levels return to normal after 48 hours.
myocardial infarction
- ECG changes
can include ST elevation, ST depression, hyperacute (peaked) T waves, T-wave inversion, new left bundle branch block, and pathologic Q waves or poor R wave progression (evolving or old transmural infarct).
ECG localization of STEMI
- V1–V2
- V3–V4
- V5–V6
- I, aVL
- II, III, aVF
- V7–V9, ST depression in V1–V3 with tall R waves
Anteroseptal (LAD)
Anteroapical (distal LAD)
Anterolateral (LAD or LCX)
Lateral (LCX)
InFerior (RCA)
Posterior (PDA)
Myocardial infarction complications
- Cardiac arrhythmia
- Postinfarction fibrinous pericarditis
Occurs within the first few days after MI. Important cause of death before reaching the hospital and within the first 24 hours post-MI.
Occurs 1–3 days after MI. Friction rub.
Myocardial infarction complications
- Papillary muscle rupture
- Interventricular septal 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.
Occurs 3–5 days after MI. Macrophage-mediated degradation VSD High O2 saturation and
pressure in RV.
Myocardial infarction complications
- Ventricular pseudoaneurysm formation
- Ventricular free wall rupture
Occurs 3–14 days after MI. Contained free wall rupture; Decrease CO, risk of arrhythmia, embolus from mural thrombus.
Occurs 5–14 days after MI. Free wall rupture leads to cardiac tamponade. LV hypertrophy and previous MI protect against free wall rupture. Acute form usually leads to sudden death
Myocardial infarction complications
- True ventricular aneurysm
- LV failure and pulmonary edema
Occurs 2 weeks to several months after MI. Outward bulge with contraction (“dyskinesia”), associated with fibrosis.
Can occur 2° to LV infarction, VSD, free wall rupture, papillary muscle rupture with mitral regurgitation.
Myocardial infarction complications
- Dressler syndrome
Occurs several weeks after MI. Autoimmune phenomenon resulting in fibrinous pericarditis.
