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).
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
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
TERMS• CARDIOMEGALY• DILATATION, any chamber, or all• HYPERTROPHY, and chamber, or all
S.A. NodeAV NodeBundle of HIS L. Bundle, R. Bundle
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.
Incidence per Million LiveMalformation Births % 4482 42Ventricular septal defect 1043 10Atrial septal defectPulmonary stenosis 836 8 781 7 Patent ductus arteriosus 577 5 Tetralogy of FallotCoarctation of aorta 492 5 396 4 Atrioventricular septal defectAortic stenosis 388 4 388 4 Transposition of great arteries 136 1 Truncus arteriosus 120 1 Total anomalous pulmonary venous connectionTricuspid atresia
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