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55 Cards in this Set

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how much does the female and male heart normally weigh
females: 250-300 gm

male: 300-350 gm
Describe the cardiac myocyte:
-ion transport
-electrical connection
-prefered energy substrate
other random stuff
-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)
normal myocyte has central nuclei, what happens during injury
during injury they get large and rectangle, he described them as "box car nuclie"
where do you measure the thickness of the ventricle
1 cm below the mitral valve
what determine CO? (what is the equation

strokevolume & heart rate
preload = EDV, what factors affect preload
1. increase with exercize, with increase in blood volume, and sympathetics.

2. decrease with venodilators
afterload = mean arteial pressure (proportional to perifpheral resistance)
vasodilators decrease afterload
what variables affect CO

Stroke Volume
what law governs wall tension
LaPlace's law = PxR / 2T

as wall thickness increases wall tension decreases\

if you dilate the ventricle tension goes up
on a cellular level what controls contractility, ultimately determining SV
-ion fluxes, membrane pumps
-actin myosin coupling
-blood flow, oxygenation, cellular energetics
- adrenergic receptors, other circulating and local factors.
on an organ level what controls contractility, ultimately determining SV
- how quickly, efficiently, forcefully the ventricle can contract

NI= 55-85%
Mod dysfxn= 30-50%
what are the 5 principle mechanisms for CV dysfunction
-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
What is the difference between heart failure and congestive heart failure
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
What clinical presntations do you see in RHF
hepatosplenomegaly, peripheral edema, and cough
pure HTN leads to what type of cardiomegaly
hypertrophy not dilation
describe the pathology
L side = concentric hypertrophy -->HTN

R side = dilation and hypertrophy -->HTN + ischemia -->cannot pump against volume
4 conditions in cardiomegaly
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
review figure
what are the 3 events that lead to heart failure and cardiac dysfxn
Valvular Dz
Myocardial Infarction
what is the definition of shock
systemic hypoperfusion often related to sudden loss of cardiac function

-many diverse forms/etiologies (see Sim center notes)
when the heart is experiencing excessive hemodynamic burden or disturbance in myocardial contractility, how does the heart compensate?
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
what is the frank starling mechanism
incrased preload of dilation enhnaces contractility (more sarcomere cross bridging) and better cardiac performance
which is most common systolic or diastolic dysfunction
systolic dysfunction
what are the 3 most common causes of systolic (left-sided) dysfunction
1 Ischemic Heart Dz
3 Aortic or mitral valve abnormalities

progressive deterioration of contractile function
name the causes of diastolic dysfunction
heart chamber can't relax and filling is compromised = restrictive heart diseases

massive L vent hypertrophy, myocardial firbrosis, amyloid deposition, constrictive pericarditis
does augementation of cardiac muscle happen by hypertrophy or hyperplasia of muscles?
hypertrophy since myocytes are terminaly differentiated they cannot undergo hyperplasia
what are the two types of congestive heart failure
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

What are the common causes of left heart failure
Ischemic heart disease, HTN, Aortic;mitral valve disease, non-ischemic myocardial disease
what happens in left heart failure
progressive damming of blood in the pulmonary circulation and diminished peripheral blood pressure/flow
what are clinical symptoms of forward failure
poor organ perfusion (especially kidneys and brain)
what are the clinical symptoms of backward failure
dyspenea and peripheral edema
List findings in left sided heart failure
LV hypertrophy, +/- dilation, fibrosis, secondary enlargement of atrium (may cause atrial fibrillation with increased risk of embolism), pulmonary congestion, edema, dyspnea, orthopnea, PND, cough
what do you see in the lungs with congestion and edema
sideroblasts (heart failure cells),, kerley B lines on xray, dyspnea, orthopnea, paroxsymal nocrurnal dyspnea
what causes kerley b lines on xray
perivascular and interstitial transudate
what is paroxsymal nocturnal dyspnea
attacks of "suffocation" when lying down at night
decreased renal perfusion leads to what?
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
Right sided heart failure is most commonly due to
secondary to left sided heart failure, causing increased pulmonary pressure
how does the congestion inthe RHF compare with LHF
it is very minimal with RHF, the "congestion" in RHF occurs as engorgemnet of systemic and portal venous systems, giving ascites and anasarca
RHF causes what findings int he liver
passive centrilobular congestion (and possibly necrosis if concurrent with LHF ischemia)

affected centrilobular areas can become fibrotic

periportal areas usually spared
what is pure RHF due to
cor pulmonade due to severe and chronic pulmonary HTN
what is nutmeg liver
the combination of mottled appearance due ot retrograde congestion and hemorrhagic plus ischemic necrosis

**NOT portal tracts
which sided heart failure causes each lung finding listed below:

1. pulmonary effusion

2. pulmonary edema
1pulmonary effusion = RHF

2pulmonary edema = LHF
what is massive generalized edema called
what other lung disease can cause RHF
COPD, diffuse lung dz, pulmonary emboli, sarcoidosis
what is the progression in RHF
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
what is cardiac cirrhosis
subsequently to centrilobular necrosis you get central fibrosis
heart failure is usually a biventricular process secondary to chronic cardiac decompensation resulting in combined effects and symptoms
random slide at end of this lecture that i couldnt come up with a question for
describe the pathology
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
besides predisposing to CHF, what is also an independent risk factor for sudden death?
Left Vent Hypertrophy
how does hyperthyroidism trigger tachycardia
stimulation of beta-adrenergics
what causes the following heart weights:

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
contrast hypertrophy due to pressure vs volume overload
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
what are other abnormalities in both types of hypertrophy
decreased capillary to myocyte ration

increased fibrotic tissue

abnormal protein deposition
what are predictable and sequential lung findings in CHF
perivascular and interstitial transudate, edematous widening of alveolar septa, alveolar space edema
what are 5 principal mechanisms that cause cardiovascular dysfunction and give examples of each
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
LO - compare teh hypertrophy of the trained heart athletic heart with that of the failing heart
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