Flashcards in The Cardiac Cycle 2: Heart Sounds and Perfomance Deck (33):
2 broad causes of heart sounds?
Rapid acceleration /deceleration of blood flow (e.g. valve closing).
Turbulent (high velocity) blood flow.
What causes the first heart sound - S(1)?
AV valve (mitral and tricuspid) closure.
What causes the second heart sound - S(2)?
Closure of the semilunar valves.
What effect does inspiration have on S(2)?
Inspiration -> increased systemic venous return -> prolonged RV ejection -> delay of pulmonic valve closure.
This delay can result in "splitting" of S2 into 2 sounds.
What are S(3) and S(4)?
Both are from ventricular filling.
S(3): Early rapid ventricular filling. (hard to hear normally)
S(4): Late rapid ventricular filling from atrial contraction (very hard to hear).
What produces heart murmurs, generally?
Turbulent flow due to abnormally high flow velocity.
(recall Reynolds relationship)
Outflow tract obstructions (aka. stenosis), AV valve regurgitation, and interventricular communications would all produce what kind of murmur?
Systolic (ejection) murmur.
AV valve obstruction and semilunar valve regurgitation would both produce what kind of murmur?
Diastolic (ventricular inflow) murmur.
If you hear a systolic murmur with a split S(2), what's one thing that could cause this?
Interventricular septum defect:
LV -> RV flow causes murmur.
Excessive RV filling delays pulmonic valve closure -> S(2) splitting.
Stroke Volume * Heart Rate = ?
2 broad factors determining stroke volume?
End diastolic volume.
Force opposing ventricular ejection.
What are the two most important parameters affect ventricular performance?
What is "preload"?
The force available to distend the myocardium at the end of diastole.
(related to ventricular end diastolic pressure)
What does the Frank-Starling Law of the Heart say?
The biggest factor affecting cardiac output is venous return.
2 parameters preload affects?
Volume available for ejection.
Contractile force that myocardium can generate.
What's the theoretically maximum % shortening of cardiac sarcomeres?
(usually it's more like 10-20%, though)
What accounts for cardiac myocytes' DIASTOLIC force-length relationship? Linear or not?
What accounts for cardiac myocyte's END SYSTOLIC force-length relationship? Is it linear or not?
Inotropic state (i.e. [Ca++]).
What is the definition of ventricular preload? What measure correlates with it?
The distending force present in the ventricle available to fill its volume at end diastole.
Ventricular end diastolic pressure (LVEDP) is used to assess preload... but there's more to it than that.
What does preload meet for sarcomere shortening, contractile strength, stroke volume, and systemic arterial pressure?
Greater stroke volume.
Greater systemic arterial pressure.
Why is too much preload a bad thing?
Too much atrial pressure = edema, either systemic or pulmonary.
What's a normal LVEDP in mmHg? How would this change in left ventricular hypertrophy?
normal LVEDP: 10-12mmHg
In hypertrophy, it increases due to reduced ventricle compliance.
Do all cardiac myocytes shorten the same amount?
Nope. Endocardial myocytes contract more - this creates the effect of the heart wall thickening during contraction.
What is the definition of afterload?
The load that ventricular muscle must overcome during systole in order to eject.
(in the left ventricle, correlated with systemic arterial pressure, but again, that's not the whole story)
How does increasing afterload affect stroke volume?
Increasing afterload decreases stroke volume.
What does LaPlace tell you about the force (i.e. tension) on/from the ventricle wall during contraction?
As the volume decreases during contraction, the ventricle doesn't need to exert as much force to maintain the same pressure.
What is inotropy?
Inotropy refers to the fact that cardiac myocytes can alter their contractile strength for a given length. (based on inputs from autonomics, heart rate, metabolic state, etc.)
End diastolic volume (EDV) - end systolic volume (ESV) = ?
Stroke volume (SV)
For each preload and afterload, it's not just the pressure in the ventricle at end diastole/systole, it's also...
the force-length relationship at that time.
2 major determinants of (end stroke volume) ESV?
If diastolic volume (aka preload) increases, what will happen to the degree to which the myocardium can shorten?
The myocardium will shorten more, and stroke volume will increase.
If afterload increases, what will happen to the myocardium's ability to shorten?
The myocardium will shorten less, decreasing stroke volume.