6.9 Cardiac Pathology Flashcards
Normal Heart
90% of mass is cardiac muscle,
very special inexhaustible muscle,
pumps 6000 litres of blood daily,
relies on coordination contractions and functions of valves
Clinical presentation of heart disease
arrhythmias,
congestive heart failure,
chest pain,
abnormal heart sounds
Branches of circumflex
marginal M1 and M2
Branches of LAD
diagonal D1, D2, D3
How is coronary artery dominance determined
the artery that supplies the posterior decending artery.
If the PDA is supplied by the right coronary artery (RC) then the coronary circulation can be classified as “right-dominant”.
If the PDA is supplied by the circumflex artery, a branch of the left coronary arter, then the coronary circulation can be classifed as “left -dominant”
Branches of the Left coronary
LAD–> diagonal branches (D1, D2),
septal branches,
Circumflex –>Marginal branches (M1, M2)
Branches of the Right coronary
Acute marginal branch,
AV node branch,
Posterior decending artery (PDA)
the right coronary
supplys blood to the right ventricle,
the RCA supplies 25% to 35% of the left ventricle (LV),
The RCA also supplies the SA nodal artery in 60% of pts
(the other 40% of the time, the SA nodal artery is supplied by the left circumflex artery)
the PDA off of the right coronary (usually)
supplies the
inferior wall,
ventricular septum, and the
posteromedial papillary muscle.
Papillary muscles
there are 5 papillary muscles in the heart,
3 in the right ventricle and
2 in the left,
the papillary muscles attach the mitral valve and the tricuspid valve to the wall of the heart,
Right–>anterior, posterior, and septal papillary muslces each attach via chordae tendinae to the tricuspid valve;
Left –> anterior and posterior papillary muscles attach via chordae tendinae to the mitral valve
What is the significance of the papillary muslces
bc there is only 2 papillary muscles on the left side, the left will fail faster
If the papillary muscles are damaged it leads to
mitral regurgitation and tricuspid insufficiency or tricuspid regurgitation
supply of the anterolateral papillary muscle
more frequently receives two blood supplies:
left anterior descending (LAD) artery and the
left circumflex artery (LCX)
—> thus it is more frequently resistant to coronary ischemia
supply of the posteromedial papillary muslce
usually supplied only by PDA –> this makes the posteromedial papillary muscle significantly more susceptible to ischemia.
The clinical significance of this is that a myocardial infarction involving the PDA is more likely to cause mitral regurgitation.
MI involving the PDA is more likely to cause
mitral regurgitation
histologically what is distinct about cardiac myocytes
nuclei are very round and you have interdigitations. Nuclei are also more centrally located
What part of the tissue in the heart is most prone to ischemia
endocardium is the furthest away from blood supply so more prone to damage and ischemia
Wiring of the heart
SA node –> AV node –> AV bundle –> AV bundle branches –> purkinje
In an MI what do you damage
you damage the part that is supplied by the vessel that is infarcted. In the heart most of the tissue is muscular, but you also have the wiring of the heart like the SA node, AV node, etc that can be damaged too
Hows is the musculature of the valves arranged
valves – chordae tendinae – papilarry muscles – ventricular wall
How dies the heart respond to changes in demande
the heart responds to demand from the rest of the body mostly by intrinsic mechanisms like hypertrophy, hyperplasia, atrophy, anaplasia, dysplasia, and also will dialate —-but failure to adapt leads to death via apoptosis or necrosis
how are the muscle fibers arranged in the heart
you have a myosin ford with a myosin light chain and myosin heavy chain, and you have actin fibers with Troponin I, C, and C, alpha tropomyosin, and Myosin binding protein C.
How do you monitor heart damage in the blood
when you have damage to the heart, some of the proteins in the arrangement of muscle fibers will be released into the blood like Troponin C, I and T
Z-disc
only actin
a single muscle fiber unit is called a
sarcomere–from z disk to z disk
Myosin - actin motion
myosin head is bound to the actin filament,
ATP binds the Myosin head and releases the actin,
ATP hydrolysis to ADP and Pi causing a confirmational change in the myosin head,
Pi released allowing for myosin head binding to actin,
ADP release allowing for conformational change causing power stroke
Cardiac Dysfunction
Pump failure, obstruction to flow, Regurgitation of flow, electrical conduction disturbance, distruption of continuity
Types of hear disease
ischemic, hypertensive, valvular, Primary myocardial (non ischemic), congenital
Heart failure definition
failure to pump out all of the blood returned to the heart
Heart failure concequences
back up of blood and/or decreased perfusion of tissues
types of heart failure
left failure, right failure, forward failure, backward failure, congestion and sequelae (lungs liver), ischemia and sequelae (kidneys)
in Left-Sided Heart Failure, the morphologic and clinical effects of left-sided CHF primarily result from
progressive damming of blood within the pulmonary circulation, and the concequences of diminished peripheral blood pressure and flow
Morphology of LHF
findings in the heart depend on the underlying disease,
Left ventricle is usually hypertrophied and often dialated, sometimes quite massively (except in mitral stenosis),
nonspecific changes of hypertrophy and fibrosis in the myocardium,
secondary enlargement of the left atrium with resultant atrial fibrillation,
can reduce stroke volume or lead to blood stasis and thrombus formation,
fibrillating left atrium carries a substantially increased risk of embolic stroke,
The extracardiac effects of lef-sided heart failure are manifested most prominently in the lungs
In what circumstance of LHF do you not see a massively hypertrophied or dialated heart
mitral stenosis
Virchow’s triad
stasis, hypercoaguability, endothelial injury –blood damming coincides with virchov’s triad and you can get thrombus formation
What is the effect of inablity to pump out all the blood in the left ventricle in LHF
increased pressure in the pulmonary veines and capillaries leading to pulmonary congestion and edema. The lungs are heavy and boggy.
Histologically what do you see in LHF
perivascular and interstitial transudate,
alveolar septal edema, and
intra-alveolar edema,
In LHF what does the pulmonary capillary leak lead to
capillary leak leads to accumulation of erythrocytes (containing hemoglobin) that are phagocytosed by machrophages. Within macrophages, hemoglobin in converted to hemosiderin (but this takes 24hr….NOT seein in early changes), Hemosiderin-containing macrophages in the alveoli (called heart failure cells) are evidence of prior pulmonary edema.
Clinical features of LHF
Dyspnea, cough, orthopnea, PND, cardiomegaly, tachycardia, a third heart sound (S3), Fine rales, systolic murmur, atrial fibrillation
Dyspnea in LHF
the earliest and most significant complaint of pts in left-sided heart failure
Cough in LHF
is also a common accompaniment of LHF due to fluid transudation in air spaces
Orthopnea in LHF
further cardiac impairment: dysnea when recumbent, this occurs bc of increased venous return from the lower extremities and by elevation of the diaphragm when in the supine position. Orthopnea is typically releved by sitting or standing, so that pts usually sleep while upright.
PND in LHF
paroxymal nocturnal dyspnea –dificulty breathing in the night when you are sleeping. A particularly dramatic form of breathlessness awakening pts from sleep with attacks of extreme dyspnea bordering on suffocation. you need to get up. You are relieve bc fluid goes down but remember it goes down slowly.
Other manifestations of LHF
Cardiomegaly, tachycardia, a third heart sound (S3)
Sounds in the lungs in LHF
rales, crackles, ronchi at the lung bases, produced by respirations through edematous pulmonary alveoli
in LHF with progressive ventricular dialation
the papillary muscles are displaced laterally, causing mitral regurgitation and a systolic murmur
In LHF, subsequent chronic dialation of the Left atrium is often associated with
atrial fibriallation, manifested by an irregularly irregular heart beat that you cannot predict and the pt can die
Lungs histology in LHF
fill of fluid (we tell by an increased specific gravity in exudate)
Right sided heart failure usually occurs
as a concequence of left sided heart failure. Any pressure increase in the pulmonary circulatioin inevitabley produces an increased burden on the right side of the heart.
Isolated right sided heart failure
is less common and it occurs in pts with
intrinsic disease of lung parenchyma and/or
pulmonary vasculature that result in chronic pulmonary hypertension (cor pulmonale)
—heart fails from lung diease but then you get pulmonary hypertension as a result;
can also occur with pulmonic or tricuspid valve disease;
congenital heart diseases with right-to-left shunt can cause isolated right-sided heart failure as well
Morphological changes in isolated RHF
hypertrophy and dilation are generally confined to the right ventricle and atrium,
bulging of the ventricular septum to the left can cause dysfunction of the left ventricle,
the major morphologic and clinical effects are engorgemtn of the systemic and prtal venous systems ( you don’t see any or see minimal pulmonary congestion)
– you’ll see pitting edema and ascities
When you see hypertrophy in the heart what do you know
you are working against an increased end diastolic volume (EDV) and you’ll have a high ejection fraction
liver has 3 zones
1–periportal,
2–midzona,
3–centrilobular (this one is more prone to ischemia bc it is furthest away from blood supply)
Microscopic architecture of liver parenchyma
both a lobule and an acinus are represented. The calssical hexagonal lobule is centered around a central vein, also known as terminal hepatic venule, and has portal tracts at three of its apices. Regions of the lobule are generally referred to as “periporta:, “midzonal”, and “centrilobular”, according to their proximity to protal spaces and central vein. Using blood supply as a source of reference, a triangular acini can be recognized. On the basis of distance from the blood supply, the acinus is divided into zones 1 (closest to blood source), 2 and 3 (farthest from blood source)
Morphology Liver and Portal System in RHF
the liver usually increases in size and weight – congestive hepatomegaly. Cut section displays prominent passive congestion, a pattern referred to as nutmeg liver. Congested red centers of the liver lobules are surrounded by paler, sometimes fatty, peripheral regions. In some instances, especially when left-sided heart failure is also present, severe central hypoxia produces centrilobular necrosis along with the sinusoidal congestion. With long-standing severe right sided heart failure, the central areas can become fibrotic, creating so-called cardiac cirrhosis.
Nutmeg appearance of the liver in RHF
heterogeneous appearance of light and dark patches. There is an area of hypoxia that undergoes necrosis, that area is light. Dark spot has blood or congested sinusoids. In the light spots you find that you’ll see that within the first 6 hours. Fatty change in the first 6 hours damaging lipid metabolism creating a white spot that undergoes necrosis giving nutmeg changes in the liver.
other changes seen in RHF
congestion of the spleen (it will be large and congested)
anatomy of the venous drainage
GI drains into portal vein (a large part of the blood supply to the liver along with the hepatic arteries) and the portal vein breaks down into the sinusoids, the sinusoids reconverge to the central vein, and the central vein combine to form the hepatic vein that join the venacava
Morphology of Liver and Portal system in RHF
RHF also leads to elevated pressure in the portal vein and its tributaries, congestion produces a tense, enlarged spleen (congestive splenomegaly), with long standing congestion, the enlarged spleen can achieve weights of 300 to 500gm (normal < 150gm)
Microscopic changes in liver and portal system due to RHF
there can be marked sinusoidal dilation, chronic edema of the bowel wall may interfere with absorption of nutrients, accumulations of transudate in the peritoneal cavity can cause ascites
Clinical features of Congestive heart failure
while the symptoms of left-sided heart failure are largely due to pulmonary congestion and edema, pure right-sided heart failure typically causes very few respiratory symptoms. Instead, there is systemic and portal venous congestion, with hepatic and splenic enlargement, peripheral edema, pleural effusion, and ascites. In most cases of chronic cardiac decompensation, pts present with biventricular CHF, encompassing the clinical syndromes of both right-sided and left-sided heart failure. As CHF progresses, pts can become frankly cyanotic and acidotic, as a result of decreased tissue perfusion
