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Flashcards in Cardiac Cycle Deck (22):


mitral valve and tricuspid valve closure; loudest at mitral area



aortic and pulmonary valve closure


what marks beginning of systole? end?

S1 is the beginning; S2 marks the end

* has isovolumetric contraction phase, rapid ejection and rduced ejection phase


JVP ⇒ a wave

atrial contraction ⇒ is the increase in atrial pressure caused by atrial systole; occurs just before S1


JVP ⇒ c wave

caused by the closed tricuspid valve bulging into the atrium due to RV contraction during systole


JVP ⇒ v wave

increased R atrial filling due to filling against closed tricuspid valve


S3 (when heard and why; when in cycle is it heard)

heard in early diastole during rapid ventricular filling phase; this is just after S2


what two pop. have a normal S3?

children and pregnant women


a pathologic S3 is associated with what general issue

increased filling pressures ⇒ common in dilated ventricles


4 conditions specifically a pathologic S3 is heard

1. dilated cardiomyopathy
2. CHF
3. Mitral regurgitation
4. L → R shunts


S4 (what causes, when in cycle is it heard)

due to "atrial kick" in late diastole, last push to get all blood out of ventricle; just before S1


what general condition makes S4 louder?

stiff ventricles→ having to push harder to get all blood out


4 specific conditions that can cause a pathologic S4

1. hypertrophic cardiomyopathy
2. Aortic stenosis
3. chronic HTN with Left vent. hypertrophy
4. post-MI → can be a sign someone has had one!


on the pressure volume loop, what happens to the graph with ↑ afterload (like in HTN)

*what happens to SV and ESV

graph gets taller and skinnier; more force being used just to overcome the systemic pressure so theres not much more energy for systolic ejection when the pressures finally get high enough to open aortic valve

* ↓ SV and ↑ ESV


what happens to the pressure volume loop with ↑ contractility? what hapens to SV, EDV and EF

gets taller and wider on the left side ⇒ ↑ SV and ↓ EDV; EF thus increases

* the right side of the graph is the same as baseline


what happens to the pressure volume loop with ↑ preload? What variable changes

gets wider to the right, but everything else stays the same⇒ increasing width on the x-axis means ↑ SV (due to ↑ EDV, but ESV is same as baseline)


what is normal splitting? which heart sound and which valve closes first and why? w/ expiration or inspiration?

on INSPIRATION, the ↓ in intrathoracic pressure allows more venous return, so the left ventricle gets more volume than the right. Thus it takes the right ventricle longer to close and during S2, the aortic valve closes first and the pulmonary second


what is wide splitting in general? which heart sound?

splitting of S2, with aortic valve closing first, like normal inspiratory splitting, but occurs during expiration as well (not normal)


what issue in general causes wide splitting? two examples?

anything that delays RV emptying
1. pulmonic stenosis
2. right bundle branch block


What is fixed splitting? what condition is it due to?

increased RA and RV volumes such that regardless of breath, pulmonic closure is delayed and S2 is split (aortic first)⇒ seen in ASD! (L to R shunt). Split is wider than in wide splitting


what is paradoxical splitting and when can it be heard in breathing cycle? what general condition causes it

normal splitting is reversed, so on expiration⇒ P2 sound is heard first. Due to conditions that delay LV emptying. On inspiration (when normal splitting should be there), the split paradoxically decreases (P2 still abnormally closing first)
* split decreases, due to the ↑ RV volume on inspiration; allows the A2 to almost catch up


2 conditions that can cause a paradoxical split

1. aortic stenosis
2. left bundle branch block

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