Path Block 2- Heart Failure And Hypertensive Heart Disease

Front 1

normal heart

Back 1

-weighs 250-350g
-RV: 0.3-0.5cm
-LV: 1.3-1.5cm

Front 2

heart conduction system

Back 2

-SA node: junctionbtw RA appendage and SVC
-AV node: RA along septum
-Bundle of His: from RA to top of ventricular septum

Front 3

myocardium

Back 3

-branching, striated, anastomosing muscle
-sarcomere=functional contractile unit

Front 4

Frank-Starling mech

Back 4

-longer lengths of sarcomeres enhance contractility (up to a point)
-moderate ventricular dilation during diastole increases subsequent force of contraction during systole

Front 5

LAD supplies...

Back 5

-apex
-ant 2/3 of septum
-ant wall of LV

Front 6

LCA supplies...

Back 6

-lateral wall of LV

Front 7

RCA supplies...

Back 7

-post 1/3 of septum
-post basal wall of LV
-RV free wall

Front 8

what do most people have as dominant circulation?

Back 8

-right sided
-determined by where PDA comes off of

Front 9

what is the region of the heart most susceptible to ischemia?

Back 9

-subendocardium

Front 10

what can cause cardiac dysfunction

Back 10

-pump failure (most common)
-obstruction to blood flow
-regurgitation
-shunted flow
-conduction defects (arrhythmias)
-disruption of continuity of circulatory system

Front 11

pump failure and cardiac dysfunction

Back 11

-most common cause of cardiac dysfunction
-weak contraction (systolic dysfunction)
or
-inadequate relaxation (diastolic dysfunction)

Front 12

obstruction to flow and cardiac dysfunction

Back 12

-pressure overload
-dt valvular stenosis or HTN

Front 13

CHF

Back 13

-failure to pump at a rate that meets the needs of active tissues
-or can only do so at an increased filling pressure (Starling mech)

Front 14

mechanisms of CHF

Back 14

-usually a slowly developing intrinsic deficit in contraction
-abnormal load presented to heart
-impaired ventricular filling
-obstruction dt valve stenosis

Front 15

causes of abnormal load presented to heart

Back 15

-acute: fluid overload, MI, valve dysfx
-chronic: ischemic heart disease, dilated cardiomyopathy, HTN

Front 16

causes of impaired ventricular filling

Back 16

-acute: pericarditis or tamponade
-chronic: restrictive cardiomyopathy, severe LV hypertrophy

Front 17

causes of obstruction dt valve stenosis

Back 17

-chronic: rheumatic valve disease (usually mitral valve)

Front 18

systolic dysfunction

Back 18

-progressive deterioration of contractile function (LV failure)
-dt ischemic heart disease, pressure or vol overload, or dilated cardiomyopathy)

Front 19

diastolic dysfunction

Back 19

-inability of heart to relax, expand, and fill sufficiently during diastole
-dt massive LVH, amyloidosis, myocardial fibrosis, constricitive pericarditis

Front 20

CHF compensatory mechanisms

Back 20

-Frank-Starling (inc preload dilation)
-Activation of neurohumoral systems
-cardiac hypertrophy

Front 21

Frank-Starling as a compensatory mech for CHF

Back 21

-increasd preload dilation helps to sustain cardiac performance by enhancing contractility (lengthened fibers contract more forcibly)
-does also inc wall tension and inc O2 requirements

Front 22

Activation of neurohormonal systems as a compensatory mech for CHF

Back 22

-release of NE by cardiac nerves: inc HR, myocard contractility, inc vascular resistance
-activate renin-angi-aldo system: inc Na and H2O reabsorption, inc CO and inc vasoconstriction
-release ANP: secreted when atrium is dilated, causes vasodilation and diuresis

Front 23

variance of hypertrophy with underlying cause

Back 23

-600g: pulm HTN and ischemic heart disease
-800g: systemic HTN, aortic stenosis, mitral regurg, dilated cardiomyopathy
-1000g: aortic regurg, hypertrophic cardiomyopathy

Front 24

concentric hypertrophy

Back 24

-indicates pressure overload
-dt HTN, aortic stenosis

Front 25

eccentric hypertrophy (hypertrophy and dilitation)

Back 25

-indicates volume overload
-dt mitral or aortic regurgitation

Front 26

Sustained cardiac hypertrophy often evolves to...

Back 26

cardiac failure

-inc myocyte size--> red capillary density
-higher O2 consumption
-altered gene express and proteins
-loss of myocytes dt apoptosis

Front 27

Left sided heart failure

Back 27

-dt progressive damming of blood within pulm circulation and diminished periph blood pressure and flow

Front 28

causes of L heart failure

Back 28

-ischemic heart disease
-HTN
-aortic and mitral valve diseases
-non-ischemic myocardial diseases (cardiomyopathies and myocarditis)

Front 29

L heart failure heart morphology

Back 29

-LVH and often dilation (often results in mitral valve insuff)
-secondary enlargement of L atrium --> a fib --> stagnant blood in atrium --> thrmobus, embolic stroke

Front 30

L heart failure lung morphology

Back 30

-inc pressure in pulm veins (transmitted to capillaries and arteries)
-pulm congestion and edema
-heart failure cells (hemosiderin-laden mac's)
-dyspnea, orthopnea, paroxysmal nocturnal dyspnea
-rales

Front 31

heart failure cells

Back 31

-hemosiderin-laden mac's in lungs
-seen with L sided heart failure

Front 32

L heart failure kidney morphology

Back 32

-dec renal perfusion activates renin-ang-aldo system --> inc blood vol
-if perfusion deficit is severe: prerenal azotemia

Front 33

L heart failure brain morphology

Back 33

-cerebral hypoxia and encephalopathy
-secondary to ischemia

Front 34

R sided heart failure

Back 34

-dt engorgement of systemic and portal venous sytems

Front 35

R sided heart failure causes

Back 35

-usually secondary to L failure
-pulm HTN
-primary myocardial disease
-tricuspid or pulm valve disease

Front 36

R heart failure heart morphology

Back 36

-RV hypertrophy and dilatation

Front 37

R heart failure liver and portal system morphology

Back 37

-elevated pressure in portal vein leads to congestive hepatosplenomegaly, cardiac cirrhosis, ascites

Front 38

R heart failure kidney morphology

Back 38

-congestion, fluid retention, periph edema
-azotemia is more pronounced than with L failure

Front 39

R heart failure brain morphology

Back 39

-venous congestion
-hypoxic encephalopathy

Front 40

R heart failure edema

Back 40

-peripheral edema (at ankle, presacral)
-eventual anasarca

Front 41

azotemia

Back 41

-R heart failure: venous congestion of kidneys
-L heart failure: less severe, lack of nutrient supply to kidney is less severe than lack of metabolite removal

Front 42

systemic vs pulmonary HTN, which side is affected?

Back 42

-systemic: L
-pulmonary: R

Front 43

systemic HTN

Back 43

-concentric LVH in absence of other CV pathology
->140/90
-25% of US population
-cardiomegaly
-LV thickness impairs diastolic filling and causes LA enlargement and mitral insuff
-myocyte hypertrophy

Front 44

systemic HTN possible clinical outcomes

Back 44

-normal longevity
-progressive ischemic heart disease
-progressive renal damage or stroke
-progressive heart failure
-sudden cardiac death

Front 45

pulmonary HTN

Back 45

-RV hypertrophy/dilatation
-acute causes: massive PE (dil of RV without hypertrophy)
-chronic causes: 1* pulm HTN or secondary pulm HTN dt chronic lung diseases