<strong>Path</strong> <strong>Cardio</strong> <strong>Outline</strong>CONGENITAL DEFECTSDisease Type Cause/Character SymptomsAtrial SeptalDefectL RShuntVentralSeptal DefectPatentDuctusArteriosisTetralogy ofFallotTranspositionGreatArteriesTruncusArteriosisTricuspidAtresiaCoarctationof AortaL RShuntL RShuntRLShuntRLShuntRLShuntRLShuntObstructHole between the atria allowing oxygenated blood into rightventricle. Most common defect to occur alone, not the mostcommon in general. More commonly occurs in the SeptumSecundum (90%) and sometimes in Septum Primum (10%)Hole between the ventricles allowing oxygenated blood intoright ventricle. Most common defect in the heart. Associatedwith Down’s Syndrome. Presents with a systolic murmurHole between the aorta and pulmonary artery allowing ↑O 2blood into lungs. Kept open with prostaglandin, closed withindomethacin. Causes a continuous machine‐like murmurRVH, Subpulmonary Stenosis, VSD, Aorta on top of VSD.Caused by an anterosuperior movement of infundibulum.Must be surgically corrected. Look for “boot‐shaped heart” inthe vignette, or cyanosis relieved by squatting (↑TPR)Swapping of aorta to RV and pulmonary artery to LV, requiringcommunication (PDA) for life. Requires surgical correction. Ifno surgery, is fatal in 1 st month of life. Occurs in diabeticmothers (but NOT in diabetes of pregnancy)Pulmonary artery and aorta do not separate, so are one bigoutflow vessel allowing mixing of blood in both directions.RA and RV do not communicate, requires ASD and VSD for life.The tricuspid valve never forms a holeInfantile = Coarctation proximal major branches (fatal)Adult = Coarctation distal major branches (found as a kid)Occurs in Turner Syndrome. Look for rib notching.Aortic Atresia Obstruct Stenosis or Atresia from something being in the way of leftventricular outflowPulmonary Obstruct Stenosis or Atresia from something being in the way of rightAtresiaventricular outflowPulmonary hypertension,Pulmonary Vasculitis, Latestage reversal of shunt =cyanosis and fatality, calledEisenminger’s Syndrome. TheRV will hypertrophy and/orpulmonary artery will stenose,reversing the flow to RLBaby is initially pinkBlue baby syndrome, occursearly in life, deoxygenatedblood gets into systemicvasculature causing cyanosis.High mortality rate, requiringsurgical intervention. Right toleft shunts will not reverse.Baby is initially blueVariable on PDA and extent ofcoarctation, usually distalcyanosis or weak pulse (feet)Atresia = Hypoplastic LVStenosis = LVHRight ventricular hypertrophyand Pulmonary DilationGROSS CHANGES FOLLOWING MISurvival Time Predominant Finding0‐24 hrs No Change1‐3 Days Yellow Pallor in the center3 Days – 4 weeks Yellow Pallor with surrounding Hyperemia6 Weeks + White/Grey Firm ScarHISTOLOGIC CHANGES FOLLOWING MISurvival Time Predominant Finding1‐4 hrs Wavy Myocytes and contraction bands4‐24hrsCoagulative Necrosis with few Neutrophils, No Myocyte Nuclei, All Pink1‐3 Days Coagulative Necrosis with many Neutrophils increasing in number3‐7 Days Coagulative Necrosis with Macrophages10+ Days Collagen Deposition, Fibroblasts, Macrophages, Granulation TissueRISK FOLLOWING MISurvival Time Predominant Finding0‐1 hrs Fatal Arrhythmia, usually Ventricular Fibrillation or Ventricular Tachycardia1‐7daysVentricular Rupture (Septal Wall or Ventricular Wall) Hemopericardium Death7+ Days Ventricular Aneurysm (no rupture, just outpouching, leading to mural thrombus)32 | O wl Club Review Sheets
33 | O wl Club Review Sheets<strong>Path</strong> <strong>Cardio</strong> <strong>Outline</strong>
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