Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
28 Cards in this Set
- Front
- Back
|
What characteristic is most clinically important for S1 versus S2?
|
Variations in...
- INTENSITY (S1) - SPLITTING (S2) |
|
|
What is physiologic splitting of S2?
|
During INSPIRATION: widening of interval between A2 and P2
- pooling of blood in lungs --> less venous return to L heart --> anticipated closure of Aortic Valve - lower intrathoracic pressure --> greater venous return to R heart --> greater R systole --> delayed closure of Pulmonic Valve During EXPIRATION: narrowing of interval between A2 and P2 |
|
|
Which semi-lunar valve closes first and why?
|
AORTIC - bc greater systemic pressure than pulmonic pressure
|
|
|
What types of EXPIRATORY S2 splitting are there? Are they pathologic?
|
Wide Physiologic Splitting - normal in young; abnormal over 50
Fixed Splitting - abnormal Paradoxical Splitting - abnormal |
|
|
What is wide physiologic splitting of S2, and what causes it?
|
= when splitting is so great that it occurs THROUGHOUT respiration (not just in inspiration, although inspiration still more evident)
Causes: 1. delayed pulmonic valve closure 2. premature aortic valve closure 3. both |
|
|
What causes a delayed pulmonic valve closure?
|
Complete Right Bundle Branch Block
- *most common - delays depolorization of R ventricle and pulmonic valve closure Severe Impedence to R ventricular emptying, such as: - Pulmonic Stenosis - Massive pulmonary embolism - Cor Pulmonale with R ventricular failure |
|
|
What causes a premature aortic valve closure?
|
Rapid emptying of L ventricle (*most common), due to:
- Severe mitral regurgitation - Ventricular septal defect Severe Congestive Heart Failure - bc reduces L ventricular stroke volume |
|
|
What is a fixed splitting of S2?
What causes it? |
S2 split remains evident throughout respiration, in both supine and upright position, and has a CONSISTENT INTERVAL between A2 and P2
Causes: - Septal defect (usually atrial), esp when ass'd with pulm hypertension - Severe impedence to R ventricle emptying - can't cope with increased R venous return on inspiration by pumping out of R vent all at once, so maintain the splitting throughout respiration |
|
|
How does the patient's position affect S2 splitting?
|
Supine - increased venous return --> widened splitting
Upright - decreased venous return --> narrowed splitting |
|
|
What is Paradoxical Splitting of S2?
|
P2 comes before A2 (reverse of normal)
Inspiration: increased venous return to R heart --> delayed closure of pulmonary --> delayed P2 decreased venous return to L --> anticipated A2 --> NARROWING OF INTERVAL between P2 and A2 |
|
|
What causes Paradoxical Splitting of S2?
|
Delay in Aortic Closure, so A2 follows P2
**More common than early closure of Pulmonic Causes: - complete L bundle branch block (usually) - increased impedence to L vent emptying (hypertension, aortic stenosis, coarctation) - L vent dysfunction (acute ischemia, cardiomyopathy) Early Closure of Pumlonic (much less common) Causes: - Decreased R vent filling (tricuspid regurg, R atrial myxoma) |
|
|
What are the main conditions in which you would hear Paradoxical Splitting of S2?
|
- After exercise or during angina (acute decompensation of pt with CAD)
- first 3 days following an acute MI (in up to 15%) - elderly pts with hypertensiona nd underlying CAD and evidence of heart failure |
|
|
How can you differentiate btwn the 2 parts of S2?
|
Listen at base, then move stethescope to apex. Note: only A2 can be heard at the apex, bc (unless pulm hypertenstion), P2 too soft to be heard there.
Thus, if the first sound goes away, P2 precedes A2 (L bundle branch block). If the second sound goes away, A2 precedes P2 (R bundle brnch block). |
|
|
What if you can hear an S2 split at the apex?
|
Normally, P closure is too soft to be able to detect at apex, so you'd only hear A. If you hear a split, then there is probably significant pulmonary hypertension causing such a loud P2 that it is audible at the apex. Atrial septal defect is also possible.
|
|
|
What can soften A2 or P2?
|
-Emphysema
-Reduced pulmonic/systemic pressure -Reduced mobility of the semilunar valves (calcification, sclerosis) - marker for severe stenosis! |
|
|
What is the significance of a loud P2 or A2?
|
-Increased pressure in pulmonic or systemic circulation
-Also due to high output states, such as aortic regurg, atrial/ventricular septal defects |
|
|
What factors increase the loudness of S1?
|
1. Ventricular contractility
- stronger contractions --> faster rise in vent pressure --> more brisk and forceful AV closure 2. Separation of AV leaflets - farther apart leaflets --> louder closure (at time of onset of vent systole) [- short P-R causes contraction to begin when leaflets are still far apart --> loud closure] [-Large A-V pressure gradient --> keeps leaflets widely separated longer --> when pressure finally builds up, close loudly] 3. Thickness of leaflets - thicker leaflets (mitral valve stenosis) --> louder closure **But as disease progresses, leaflets become fixed and calcified, and closure becomes softer |
|
|
What 2 pathological conditions can be enhanced using the VALSALVA MENUEVER?
|
- mitral valve prolaps (also increases the length of the murmur)
- HOCM |
|
|
What are the changes in PMI/arterial pulse for aortic regurgitation?
|
- PMI displaced DOWNWARD and LATERALLY
- Single PMI - Double arterial pulse |
|
|
What are the changes in PMI/arterial pulse for mitral regurgitation?
|
- PMI displaced DOWNWARD and LATERALLY
- Double PMI (S3 becomes palpable) - Single arterial pulse |
|
|
Which is easier to detect - S3 or S4 - and why?
|
S4 - higher pitched, louder (but not quite as long)
|
|
|
What is the difference between active and passive ventricular filling?
What percent of filling occurs during each? What extra heart sounds are associated with each? |
Passive filling = 80%
- In early diastole following AV valve opening due to pressure gradient - Coincides with S3 Active Filling = 20% - In late diastole as a resuly of atrial contraction - Coincides with S4 |
|
|
What is the cause(s) of a physiologic S3?
What is the cause(s)of a pathologic S3? How can the be differentiated? |
Physiologic S3
- Healthy children and young adults - Athletes with bradycardia Pathologic S3 - ***S3 above age 40 should be considered pathologic! (until proven otherwise) - usually with tachycardia - increased ventricular preload (diastolic overload) - reduced ventricular function/"floppy" ventricular wall *Tell them apart mostly bc pathologic S3 will be associated with SYMPTOMS |
|
|
What are the clinical and overall health implications in a patient with S3?
|
Very good predictor of POOR systolic function....
-Pts with CHF, more likely to die -Pts with elevated jugular venous pressure, worse outcome -Signif risk of MI during non-cardiac surgery -Pts with mitral regurg, worse disease |
|
|
What are the clinical and overall health implications in a patient with S3?
|
Very good predictor of POOR systolic function....
-Pts with CHF, more likely to die -Pts with elevated jugular venous pressure, worse outcome -Signif risk of MI during non-cardiac surgery -Pts with mitral regurg, worse disease |
|
|
Which is more common - S3 or S4?
|
S4
|
|
|
What is the cause(s) of a physiologic S4?
What is the cause(s)of a pathologic S4? How can the be differentiated? |
***S4 is ALWAYS PATHOLOGIC***
|
|
|
How can S3 and S4 best be heard on auscultation?
|
Patient in left lateral decubitis position; use BELL and press with light pressure (firm pressure turns it into a diaphragm)
|
