Path Cardio Outline - TMedWeb

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Path Cardio OutlineAngina‐ Inflammationo The stability of a plaque is dependent on collagen and the fibrous content.o Activation of macrophages (active inflammation) results in metalloproteinases thatdegrade the collagen, weakening the fibrous cap.o C Reactive Protein is an acute phase molecule of inflammation, used as a prognosticindicator for ischemic events‐ Vasoconstrictiono Vasospasm, for whatever reason, occludes blood vessel. In a healthy vessel, this doesnothing. In an already stenosed vessel, this causes occlusion.o Responds well to nitratesThere is a spectrum of conditions that represent minor occlusion to complete occlusion. Thus, there aredifferent types of angina. While categorized in the coming section, it must be noted that there is in facta continuum of states and conditions that makes its way from stable to unstable to full blownMyocardial Infarction. Pritzmental is a special kind of angina. Angina itself is ischemic chest pain.‐ Stable Anginao Significant stenosis = 75% occlusion = decreased perfusiono Perfusion maintained while at resto Exercise or emotional stress = increase in demand = ischemic chest paino Alleviated with rest or nitrates‐ Unstable Anginao Worsening stenosis = 90% occlusion = critically decreased perfusiono Perfusion compromised while at rest or with little exertion.o Severe stenosis, thrombus, or vasospasm not alleviated by nitrates‐ Pritzmental Anginao Uncommon, irregular attacks caused by vasospasmo Responds well to nitrateso Is unrelated to physical activity, BP, stress, etcMyocardial InfarctionAn infarct occurs in an area supplied by an occluded coronary vessel. For all intents and purposes, thereis no collateral circulation in the heart, except in the case of long term, severely stenotic disease. Thewall is thick, the arteries are on the epicardial surface. Therefore, the myocytes of the endocardialsurface (called the subendocardium) are at particular risk, being farthest from the blood supply whilethe myocytes of the epicardial surface (called the subepicardium) are at least risk. Infarction results innecrosis and loss of function, unless reperfusion can be achieved in a relatively short amount of time.12 | O wl Club Review Sheets
Path Cardio Outline‐ Typeso Transmural• Complete thickness, literally “across the wall” from subendocardium tosubepicardium representing a long standing, severe ischemia• Caused by an unalleviated completely occluding thrombosis or stenosis.• Occurs in a single geographical region supplied by the occluded vesselo Subendocardial• Involves less than the full thickness (1/3 – 1/2)• Subendocardium is the least well perfused and is most vulnerable• Coronary occlusion causes single area of riskPink area representsSubendocardial infarct• Systemic hypotension may result in global ischemia of vulnerablesubendocardium throughout heartPink arearepresentstransmural infarctInverted TST ElevationQ Wave‐ Clinical Features of MIo Patient ‐ Presentation Suspects an MI• Cold, Clammy, Diaphoretic, Dyspnea, Substernal Chest Pain (visceral painexplained as a crushing) that radiates to the Jaw or down the arm• Feeling of Impending Doom – “I’m going to die!”• Diabetics, Elderly and Women may be asymptomatic (silent MI).o Electrocardiogram ‐ Screen Suspected patients for MI• Hallmark of ischemia is the T wave inversion• Hall mark of Infarct = ST Segment Elevation (Transmural) ST SegmentDepression (Subendocardial)• Hallmark of Old Infarct is Q wave ElongationoCK‐MB Troponin82,000 24,000Mol.WeightIncrease 3‐6hrs 4‐8hrsPeak 12‐24hrs 12‐16hrsReturn 24‐72hrs 5‐9daysLabs – Troponins and Ck‐MB Confirm the Diagnosis• Cardiac Troponins are the new golden standard. Unique to myocytes,detectable throughout evolution of MI. Get Troponin I• CK‐MB is former golden standard. Creatine Kinase is in brain (CK‐BB), muscle(MM) and in heart (MB). When damaged, the heart should release CK‐MB.Difficult to track, could be associated with another condition, and is onlydetectable later in evolution• Myoglobin, lactate Dehydrogenase (LDH), C reactive Protein, are usefulmarkers when the clinical picture of infarct is present. These are nonspecific formyocardium and may be elevated if the patient worked out that day13 | O wl Club Review Sheets
Page 1: Path Cardio OutlineCARDIAC FAILURET
Page 4 and 5: Path Cardio OutlineInflammationNorm
Page 6 and 7: Path Cardio OutlineOut the aorta, b
Page 8 and 9: Path Cardio OutlineRA and RV commun
Page 10 and 11: Path Cardio OutlineAortic Stenosis
Page 14 and 15: Path Cardio Outline‐ Coronary Art
Page 16 and 17: Path Cardio OutlineHYPERTENSIVE HEA
Page 18 and 19: Path Cardio OutlineCardiac Muscle
Page 20 and 21: Path Cardio OutlineRed Bumps all li
Page 22 and 23: Path Cardio OutlineoooHistologicall
Page 24 and 25: Path Cardio OutlineAtrium is dilate
Page 26 and 27: Path Cardio OutlineMedial degenerat
Page 28 and 29: Path Cardio OutlineVEINS AND LYMPHA
Page 30 and 31: Path Cardio OutlineDiseaseInfectiou
Page 32 and 33: Path Cardio OutlineCONGENITAL DEFEC

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