Heart - Dr. Nowacki Diseases Of The Heart

Front 1

how much does the female and male heart normally weigh

Back 1

females: 250-300 gm

male: 300-350 gm

Front 2

Describe the cardiac myocyte:
-ion transport
-electrical connection
-prefered energy substrate
other random stuff

Back 2

-anastomosing electrically connected gap jxns, intercalated disks
-highly organized T tubule system, SR, terminal cisternae for ion transport
- perfers Fatty Acids, long chain FFA (glucose and galactose also used)
-other: 60% contractile, 25% mito, has receptors and secretory granules (ANP)

Front 3

normal myocyte has central nuclei, what happens during injury

Back 3

during injury they get large and rectangle, he described them as "box car nuclie"

Front 4

where do you measure the thickness of the ventricle

Back 4

1 cm below the mitral valve

Front 5

what determine CO? (what is the equation

Back 5

SV x HR

strokevolume & heart rate

Front 6

preload = EDV, what factors affect preload

Back 6

1. increase with exercize, with increase in blood volume, and sympathetics.

2. decrease with venodilators

Front 7

afterload = mean arteial pressure (proportional to perifpheral resistance)

Back 7

vasodilators decrease afterload

Front 8

what variables affect CO

Back 8

SV CAP

Stroke Volume
Contractility
Afterload
Preload

Front 9

what law governs wall tension

Back 9

LaPlace's law = PxR / 2T

as wall thickness increases wall tension decreases\

if you dilate the ventricle tension goes up

Front 10

on a cellular level what controls contractility, ultimately determining SV

Back 10

-ion fluxes, membrane pumps
-actin myosin coupling
-blood flow, oxygenation, cellular energetics
- adrenergic receptors, other circulating and local factors.

Front 11

on an organ level what controls contractility, ultimately determining SV

Back 11

- how quickly, efficiently, forcefully the ventricle can contract
- Measured by** EJECTION FRACTION: SV/EDV

NI= 55-85%
Mod dysfxn= 30-50%
***SEVER DYSFXN = BELOW 30%

Front 12

what are the 5 principle mechanisms for CV dysfunction

Back 12

-pump failure - most commome
-obstuction to flow - HTN or aortic stenosis
-regurgitant flow (valvular dz)
-disorders of cardiac conduction (arrythmias) = not efficient heart
-interuption of circulation = coronary artery dz

Front 13

What is the difference between heart failure and congestive heart failure

Back 13

Heart failure is the pathophysiologic state where the heart can not deliver enough blood to the meet the needs of the body.

In contrast congestive heart failure is a syndrome that overall reflects inadequate pump function

Front 14

What clinical presntations do you see in RHF

Back 14

hepatosplenomegaly, peripheral edema, and cough

Front 15

pure HTN leads to what type of cardiomegaly

Back 15

hypertrophy not dilation

Front 16

describe the pathology

Back 16

L side = concentric hypertrophy -->HTN

R side = dilation and hypertrophy -->HTN + ischemia -->cannot pump against volume

Front 17

4 conditions in cardiomegaly

Back 17

1 is affecting the kidneys-->dying-->renal failure is coming-->Inc afterload

2 is accelerated - HTN too much for heart = dilation

3 CAD-->infarcts-->slow
myocardial scarring won't be able to pump and starts dilating
4. Massive MI - rapid increase in dz and heart failure, not pumping against system

Front 18

review figure

Back 18

what are the 3 events that lead to heart failure and cardiac dysfxn

Hint 18

Hypertension
Valvular Dz
Myocardial Infarction

Front 19

what is the definition of shock

Back 19

systemic hypoperfusion often related to sudden loss of cardiac function

-many diverse forms/etiologies (see Sim center notes)

Front 20

when the heart is experiencing excessive hemodynamic burden or disturbance in myocardial contractility, how does the heart compensate?

Back 20

Frank Starling-(inc BP) increased preload yields increased contractility-->if goes to far =heart failure

structural changes in myocardium, augmented muscle mass

activation of neurohumoral systems: norepi/ept, renin-angio-aldo, ANP

Front 21

what is the frank starling mechanism

Back 21

incrased preload of dilation enhnaces contractility (more sarcomere cross bridging) and better cardiac performance

Front 22

which is most common systolic or diastolic dysfunction

Back 22

systolic dysfunction

Front 23

what are the 3 most common causes of systolic (left-sided) dysfunction

Back 23

1 Ischemic Heart Dz
2 HTN
3 Aortic or mitral valve abnormalities

progressive deterioration of contractile function

Front 24

name the causes of diastolic dysfunction

Back 24

heart chamber can't relax and filling is compromised = restrictive heart diseases

massive L vent hypertrophy, myocardial firbrosis, amyloid deposition, constrictive pericarditis

Front 25

does augementation of cardiac muscle happen by hypertrophy or hyperplasia of muscles?

Back 25

hypertrophy since myocytes are terminaly differentiated they cannot undergo hyperplasia

Front 26

what are the two types of congestive heart failure

Back 26

Forward failure = diminished cardiac output -->can't meet demand, renal failure,ect because try to preserve Brain

Backward failure = accumulation of blood in the venous system

OR BOTH

Front 27

What are the common causes of left heart failure

Back 27

Ischemic heart disease, HTN, Aortic;mitral valve disease, non-ischemic myocardial disease

Front 28

what happens in left heart failure

Back 28

progressive damming of blood in the pulmonary circulation and diminished peripheral blood pressure/flow

Front 29

what are clinical symptoms of forward failure

Back 29

poor organ perfusion (especially kidneys and brain)

Front 30

what are the clinical symptoms of backward failure

Back 30

dyspenea and peripheral edema

Front 31

List findings in left sided heart failure

Back 31

LV hypertrophy, +/- dilation, fibrosis, secondary enlargement of atrium (may cause atrial fibrillation with increased risk of embolism), pulmonary congestion, edema, dyspnea, orthopnea, PND, cough

Front 32

what do you see in the lungs with congestion and edema

Back 32

sideroblasts (heart failure cells),, kerley B lines on xray, dyspnea, orthopnea, paroxsymal nocrurnal dyspnea

Front 33

what causes kerley b lines on xray

Back 33

perivascular and interstitial transudate

Front 34

what is paroxsymal nocturnal dyspnea

Back 34

attacks of "suffocation" when lying down at night

Front 35

decreased renal perfusion leads to what?

Back 35

activation of the renin-angio-aldo system causing retetion of salt and water giving volume expansion-->which contributes to pulmonary edema -->counteracted by ANP by atrial dilation

Front 36

Right sided heart failure is most commonly due to

Back 36

secondary to left sided heart failure, causing increased pulmonary pressure

Front 37

how does the congestion inthe RHF compare with LHF

Back 37

it is very minimal with RHF, the "congestion" in RHF occurs as engorgemnet of systemic and portal venous systems, giving ascites and anasarca

Front 38

RHF causes what findings int he liver

Back 38

passive centrilobular congestion (and possibly necrosis if concurrent with LHF ischemia)

affected centrilobular areas can become fibrotic

periportal areas usually spared

Front 39

what is pure RHF due to

Back 39

cor pulmonade due to severe and chronic pulmonary HTN

Front 40

what is nutmeg liver

Back 40

the combination of mottled appearance due ot retrograde congestion and hemorrhagic plus ischemic necrosis

**NOT portal tracts

Front 41

which sided heart failure causes each lung finding listed below:

1. pulmonary effusion

2. pulmonary edema

Back 41

1pulmonary effusion = RHF

2pulmonary edema = LHF

Front 42

what is massive generalized edema called

Back 42

anasarca

Front 43

what other lung disease can cause RHF

Back 43

COPD, diffuse lung dz, pulmonary emboli, sarcoidosis

Front 44

what is the progression in RHF

Back 44

Increase RVhypertrophy-->then dilates-->affects the valve-->atrial hypertrophy-->then dilates-->creates area prone to thrombi-->could cause PE

** once start-->gets worse
-primary pulmonary HTN is not very common

Front 45

what is cardiac cirrhosis

Back 45

subsequently to centrilobular necrosis you get central fibrosis

Front 46

heart failure is usually a biventricular process secondary to chronic cardiac decompensation resulting in combined effects and symptoms

Back 46

random slide at end of this lecture that i couldnt come up with a question for

Front 47

describe the pathology

Back 47

this is a picture of an actual nutmeg(upper left) and nutmeg liver

I have stars by this in my notes, so i would make sure to know this and the previous cards on the pathogenesis of this finding

Front 48

besides predisposing to CHF, what is also an independent risk factor for sudden death?

Back 48

Left Vent Hypertrophy

Front 49

how does hyperthyroidism trigger tachycardia

Back 49

stimulation of beta-adrenergics

Front 50

what causes the following heart weights:

-250-350
-350-600
-400-800
-600-1000

Back 50

250-350 = normal
-350-600 = (2x normal) pumonary HTN, ischemic heart dz
-400-800 = 3x normal, systemic HTN, aortic stenosis, mitral regurgitation, hypertrophyic cardiomyopathy
-600-1000 = >3x normal aortic regurgitation, hypertrophic cardiomyopathy

Front 51

contrast hypertrophy due to pressure vs volume overload

Back 51

Pressure (aortic stenosis, HTN) = concentric, parallel sarcomere deposition, cross sectional area expanded by cell length unchanged

volume (valvular dz, MI) = new sarcomeres and cell length increases giving dilation and increase wall thickness

Front 52

what are other abnormalities in both types of hypertrophy

Back 52

decreased capillary to myocyte ration

increased fibrotic tissue

abnormal protein deposition

Front 53

what are predictable and sequential lung findings in CHF

Back 53

perivascular and interstitial transudate, edematous widening of alveolar septa, alveolar space edema

Front 54

what are 5 principal mechanisms that cause cardiovascular dysfunction and give examples of each

Back 54

1. failure of pump: inadequate muslce contraction (systolic dysfxn) or relaxation (diastolic dysfxn)

2. flow obstruction: aortic stenosis, HTN, aortic coartation

3. regurgitant flow; aortic and mitral regurgitation

4. conduction disorders: heart block arrythmias

5. ciculatory disruption: blood loss, GSW

Front 55

LO - compare teh hypertrophy of the trained heart athletic heart with that of the failing heart

Back 55

yes, i know it wasn't in the notes anywhere or Robbins that I could find quickly but found this in the International Journal of Cardiology via a google search