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Heart part-1
- 1. HEART
- 2. THE HEART • Normal • Pathology – Heart Failure: L, R – Heart Disease • Congenital: LR shunts, RL shunts, Obstructive • Ischemic: Angina, Infarction, Chronic Ischemia, Sudden Death • Hypertensive: Left sided, Right sided • Valvular: AS, MVP, Rheumatic, Infective, Non-Infective, Carcinoid, Artificial Valves • Cardiomyopathy: Dilated, Hypertrophic, Restrictive, Myocarditis, Other • Pericardium: Effusions, Pericarditis • Tumors: Primary, Effects of Other Primaries • Transplants
- 3. NORMAL Features • 6000 L/day • 250-300 grams • 4 40% of all deaths (2x cancer) • Wall thickness ~ pressure • ( (i.e., a wall is only as thick as it has to be) – LV=1.5 cm – RV= 0.5 cm – Atria =.2 cm • Systole/Diastole • Starling’s Law
- 4. TERMS • CARDIOMEGALY • DILATATION, any chamber, or all • HYPERTROPHY, and chamber, or all
- 6. S.A. NodeAV NodeBundle of HIS L. Bundle, R. Bundle
- 9. VALVES • AV: – TRICUSPID 13 cm – MITRAL 11 cm • SEMILUNAR: – PULMONIC 8 cm – AORTIC 6 cm
- 10. CARDIAC AGING Epicardial Coronary Chambers Arteries Increased left atrial cavity size Tortuosity Decreased left ventricular cavity size Increased cross-sectional luminal area Sigmoid-shaped ventricular septum Calcific deposits Atherosclerotic plaque Myocardium Increased mass Valves Increased subepicardial fat Aortic valve calcific deposits Mitral valve annular calcific deposits Brown atrophy Lipofuscin deposition Fibrous thickening of leaflets Basophilic degeneration (glyc.) Buckling of mitral leaflets toward the left atrium Amyloid deposits
- 11. CARDIAC AGING Aorta Dilated ascending aorta with rightward shift Elongated (tortuous) thoracic aorta Sinotubular junction calcific deposits Elastic fragmentation and collagen accumulation Atherosclerotic plaque
- 13. Pathologic Pump Possibilities • Primary myocardial failure (MYOPATHY) • Obstruction to flow (VALVE) • Regurgitant flow (VALVE) • Conduction disorders (CONDUCTION SYSTEM) • Failure to contain blood (WALL INTEGRITY)
- 14. • DEFINITION CHF • TRIAD – 1) TACHYCARDIA – 2) DYSPNEA – 3) EDEMA • FAILURE of Frank Starling mechanism • HUMORAL FACTORS – Catecholamines (nor-epinephrine) C – ReninAngiotensionAldosterone – Atrial Natriuretic Polypeptide (ANP) A • HYPERTROPHY and DILATATION
- 15. HYPERTROPHY • PRESSURE OVERLOAD (CONCENTRIC) P • VOLUME OVERLOAD (CHF) • LVH, RVH, atrial, etc. • 2X normal weight ischemia • 3X normal weight HTN • >3X normal weightMYOPATHY, aortic regurgitation
- 17. CHF: Autopsy Findings • Cardiomegaly • Chamber Dilatation • Hypertrophy of myocardial fibers, BOXCAR nuclei
- 19. Left Sided Failure • Low output vs. congestion • Lungs – pulmonary congestion and edema – heart failure cells • Kidneys – pre-renal azotemia – salt and fluid retention • renin-aldosterone activation • natriuretic peptides • Brain: Irritability, decreased attention, stuporcoma
- 20. Left Heart Failure Symptoms • Dyspnea – on exertion – at rest • Orthopnea – redistribution of peripheral edema fluid – graded by number of pillows needed • Paroxysmal Nocturnal Dyspnea (PND)
- 21. LEFT Heart Failure Dyspnea Orthopnea PND (Paroxysmal Nocturnal D Dyspnea) Blood tinged sputum Cyanosis Elevated pulmonary “WEDGE” pressure (PCWP) (nl = 2-15 mm Hg)
- 22. Right Sided Heart Failure • Etiology – left heart failure – cor pulmonale • Symptoms and signs – Liver and spleen • passive congestion (nutmeg liver) p • congestive spleenomegaly • ascites – Kidneys – Pleura/Pericardium • pleural and pericardial effusions • transudates – Peripheral tissues
- 23. RIGHT Heart Failure FATIGUE “Dependent” edema JVD H Hepatomegaly (congestion) ASCITES, PLEURAL EFFUSION GI Cyanosis Increased peripheral venous pressure (CVP) (nl = 2-6 mm Hg) (
- 24. HEART DISEASE • CONGENITAL (CHD) C • ISCHEMIC (IHD) • HYPERTENSIVE (HHD) • VALVULAR (VHD) • MYOPATHIC (MHD)
- 25. CONGENITAL HEART DEFECTS • Faulty embryogenesis (week 3-8) F • Usually MONO-morphic (i.e., SINGLE lesion) (ASD, VSD, hypo-RV, hypo-LV) • May not be evident until adult life (Coarctation, ASD) • Overall incidence 1% of USA births • INCREASED simple early detection via non invasive methods, e.g., US, MRI, CT, etc.
- 26. Incidence per Million Live Malformation Births % 4482 42 Ventricular septal defect 1043 10 Atrial septal defect Pulmonary stenosis 836 8 781 7 Patent ductus arteriosus 577 5 Tetralogy of Fallot Coarctation of aorta 492 5 396 4 Atrioventricular septal defect Aortic stenosis 388 4 388 4 Transposition of great arteries 136 1 Truncus arteriosus 120 1 Total anomalous pulmonary venous connection Tricuspid atresia
- 27. GENETICS • Gene abnormalities in only 10% of CHD • Trisomies 21, 13, 15, 18, XO • Mutations of genes which encode for transcription factorsTBX5ASD,VSD NKX2.5ASD • Region of chromosome 22 important in heart development, 22q11.2 deletionconotruncus, branchial arch, face
Notas del editor
- Just as we said the Blood Vessel chapter was 1) atherosclerosis and 2) everything else We can now say the heart chapter is 1) ischemic heart disease and 2) everything else
- This is the chapter outline, fairly logical
- Remember 1.5 cm is considered to be the AVERAGE LV wall thickness, RV is 1/3 that, and atria are ½ RV.
- The specialized myocytes of the heart’s conduction system, Purkinje fibers, running sub-endocardially, have this unique appearance. I do not recall any pathologist ever pinpointing an EKG abnormaility to a specific histopathologic abnormality of a Purkinje fiber.
- Whichever artery winds up supplying the posterior interventricular septum is said to be “DOMINANT”. A thrombosis of WHICH coronary artery would usually result in sudden death? Ans: MAIN left coronary artery.
- The myocardial perfusion is a good test of coronary artery and myocardial function.
- These features are seen so commonly in autopsies of elderly people no matter what they died from. Also keep in mind that most people who do not die ACUTELY, die in cardiac failure.
- One very key philosophical question is whether atherosclerosis is part of aging or not. We can leave that for the philosophers.
- The pigment which accumulates with age is called lipofucsin, and caused the heart to appear “browner” than normal. This is called “brown” atrophy of the heart. Lipofucsin is another typical example of a golden brown, slightly refractile, IN trinsic pigment, which looks like hemosiderin, melanin, or bile, but accumulates, as a rule, on opposite poles of the myocyte nucleus. It is also called, appropriately, AGING pigmernt.
- This is the same analogy as the “straw” we talked about in the last chapter on blood vessels. You can classify cardiac diseases functionally into these 5 “pump” categories, like we had only 2 categories with the blood vessels described as straws or conduits.
- ANP acts to reduce the water, sodium and adipose loads on the circulatory system, thereby reducing blood pressure
- Very FEW hearts of elderly people at autopsy weigh the normal 250-300 gm. Atherosclerotic or CHF hearts weigh twice as much, hypertensive hearts weight three times as much, and cardiomyopathic hearts often weigh more.
- A good general diagram.
- Note that not only is the FIBER thick, but so are the nuclei. Note squaring off of the nuclei, so called “BOXCAR” effect.
- Can you understand why all of these findings can be related to LEFT sided heart failure? Ans: YES, primarily PULMONARY.
- Can you understand why all of these findings can be related to RIGHT sided heart failure? Ans: YES, primarily STSTEMIC.
- Does this look like it covers all bases? Ans: YES You can always logically remember heart diseases as being in one of these 5 categories.
- Do the NAMES of these congenital heart conditions adequately describe the pathology? Ans: YES Why have I highlighted the “D”s and the “T”s? Ans: D = L R shunt, T= R L shunt (cyanosis, or “blue” babies).