L17- CVS Pathology I Flashcards
Normal LV thickness?
Normal RV thickness?
LV- 10-15 mm
RV- 3-5 mm
Normal Heart Weight:
males?
females?
Males: 250-300 g
Females: 200-250 g
define the types of cardiomegaly
-Generally: an inc in cardiac weight or size
Cardiac Hypertrophy: inc weight, inc ventricular thickness
Dilation: enlarged chamber size
The weight of the heart under the following conditions:
(1) IHD
(2) HTN, AS, MS, DCM
(3) AR, HCM
1- up to 600 g (ischemic HD)
2- 400-600 g (HTN, aortic stenosis, mitral regurg., dilatated cardiomyopathy)
3- 600-1000 g (aortic regurg., hypertophic cardiomyopathy)
Pericardial cavity contains (1) amount of fluid for (2) purpose
- 30-50 mL
- acts as a shock absorber
list the layers of the heart wall (superficial to deep)
(pericardium)
- epicardium
- myocardium
- endocardium
Note- usually only distinguishable during pathological conditions
myocardium is composed of cardiac myocytes and sparse amounts of…..
- endothelial cells associated with capillaries
- fibroblasts: usually with dead heart tissues –> fibrosis
heart valves are lined with (1) layer of the heart and receive blood supply via (2)
1- endocardium
2- diffusion from heart’s blood (thin enough for process to be successful)
(T/F) coronary vessels have abundant collateral circulation
F- collaterals usually form if one or more arteries become severely narrowed, usually with hyperlipidemia, etc
Heart Hypertrophy is due to the increase in (1) and (2). (3) does not usually accompany (1) and (2), therefore the following process occurs, (4). However, (1) and (2) are coupled with an increase in (5) for the heart, resulting in (6).
1- cardiac myocyte size
2- sacromeres (actin and myosin upregulation)
3- increased vascularization
4- dec capillary density –> ischemia –> fibrosis –> reduced diastolic relaxation
5- O2/metabolic demand
6- cardiac decompensation
(1) hypertrophy occurs due to a pressure overload, as seen in (2) and (3) conditions. New sarcomeres are added in (4) fashion to existing sarcomeres, resulting in (5).
1- concentric
2/3- HTN, Aortic Stenosis (few other conditions)
4- in-parallel
5- inc wall thickness + dec diameter of cavity
(1) hypertrophy occurs due to volume overload, as seen in (2). New sarcomeres are added in (3) fashion to existing sarcomeres, resulting in (4).
1- eccentric
2- aortic regurgitation (+ most other cardiac pathologies)
3- in-series
4- muscle mass inc proportional to chamber dilation (no inc in wall thickness)
list the 5 categories of HF
1) diastolic v systolic
2) high output v low output
3) LHF v RHF
4) forward, backward failure
5) compensated v decompensated failure
Systolic HF is defined as (1) due to one of the following: (2)
1- inability to contract properly 2: -myocyte loss (MI) -Pressure overload (HTN) -Volume overload (valve regurg,) -dec contractility (myocarditis, DCM)
Diastolic HF is defined as (1) due to one of the following: (2).
1- inability of heart to relax and fill 2: -massive ventricular hypertrophy -myocardial fibrosis -amyloidosis -constrictive pericarditis
(T/F) systolic and diastolic dysfunction can both exist in a patient
T- inability to contract and fill properly can be seen
compare high and low output HF
HIGH:
- CO is normal/functioning, HF Sxs still present
- seen in inc tissues demands: anemia, hyperthyroidism, pregnancy
- systolic dysfunction
LOW:
- dec CO
- majority of cardiac diseases => low CO HF
describe forward HF
- dec output into systemic circulation
- => renal hypoperfusion –> inc RAAS –> Na/H2O retention –> edema
-low BP, fatigue, syncope, shock
describe backward HF
(LHF)
- pulmonary congestion –> pulmonary edema –> pulmonary HTN
- => RHF –> systemic venous congestion –> edema, ascites (portal HTN), raised JVP, congested liver
list the 3 compensatory mechanisms for HF
(note- if successful then its compensated HF, if unsuccessful then its decompensated HF)
1) neurohormonal systems: endogenous catecholamines, RAAS
2) myocardial hypertrophy (concentric, eccentric)
3) Frank-Starling Law: inc contractile force with myofiber stretching (b/c inc EDV)
list the Sxs of LVF
- dyspnea
- orthopnea (dyspnea while lying down)
- paroxysmal nocturnal dyspnea (dyspnea while sleeping)
list the Sxs of RVF
- systemic venous congestion: distended neck veins (jugular distension) + enlarged tender liver
- soft tissue edema
describe the morphological changes due to LHF on:
(1) heart
(2) brain
(3) kidney
(4) lungs
1- hypertrophies (mostly dilated)
2- hypoxic encephalopathy
3- ATN
4- congestion –> edema –> if chronic then brown induration (heavy + wet lungs upon gross examination: frothy mixture of surfactant and blood)
describe the morphological changes due to RHF on:
(1) liver
(2) spleen
(3) pleural, pericardial spaces
(4) soft tissues
1- chronic passive congestion –> nutmeg liver
2- enlargement + enlargement of spleen
3- pleural/pericardial effusions
4- soft tissue edema
list the five types of HD
- IHD (ischemic)
- HTN HD
- valvular HD
- non-ischemic (primary) myocardial disease
- congenital HD
define IHD
(ischemic heart disease)
- syndrome that have an imbalance between cardiac blood supply / perfusion and myocardial oxygen / nutritional demands
- also called CAD (coronary artery disease)
(1) is the number cause of mortality in US + other industrialized nations, affecting people (2) age and (3) gender most
1- IHD
2- any age, more common in older people
3- Males > Females (>80 y/o M=F)
list the 4 IHD syndromes / consequences
1) angina pectoris (severe, transient chest pain, no cell death): stable, unstable, or prinzmetal (variant)
2) acute MI (chunk of cells dead)
3) chronic IHD w/ CHD (small number of cells die, heart dilatation)
4) SCD (sudden cardiac death- usually via arrhythmias, fibrillations, conductance disturbance)
acute coronary syndrome refers to…..
- MI
- unstable angina
- SCD (sudden cardiac death)
IHD is mostly caused by (1), but can also be caused by one of the following: (2)
1- atherosclerosis (90%)
2- anemia/hypoxemia, low systemic BP / shock, inc cardiac demand (hypertrophy, exercise), vasculitis, aortic dissection
list the 4 factors apart of pathogenesis leading to IHD
1) coronary artery obstruction (fixed)
2) acute plaque changes
3) coronary intraluminal thrombosis
4) vasoconstriction
Most IHD patients (90%) will have (1) causing a (2) in coronary arteries. With progressive growth of (1), it will develop into (3), defined as a (4)% reduction in arterial cross-sectional area. Therefore (5) is insufficient enough to help meet myocardial demands leading to (6).
(coronary artery obstruction role in IHD)
1- atherosclerosis
2- stable fixed narrowing
3- critical stenosis
4- 75%
5- compensatory vasodilation
6- ischemia with exercise/exertion –> angina attacks
Mechanical stresses in the coronary arteries can cause disruption of and formation of (1). Changes to (1) morphology include one of the following: (2). Most often, changes to (1) leads to the following cascade: (3).
(acute plaque changes role in IHD)
1- unstable plaque
2- erosion, ulceration, fissuring, rupture +/- hemorrhage
3- precipitate formation of superimposed thrombus –> occlusion –> acute coronary syndrome
list the characteristics of unstable plaques
(acute plaque changes role in IHD)
- cause moderate stenosis (50-75% occlusion)
- thin fibrous cap
- core rich in lipids, macrophages, T-cells
- less evidence of smooth muscle proliferation
- markedly eccentric: not uniform around vessel circumference
list the factors that cause increased vasoconstriction in coronary vessels (therefore –> IHD)
- locally released platelet contents: TX-A2
- impaired NO secretion relative to endothelin / contracting factors
- inc adrenergic activity
- smoking (also dec Hb)
