PVLs, Wegeners, S2 Splits Flashcards
Starting from Bottom Right of the Pressure volume loop and moving counter clock-wise lable the points
1.
2.
3.
4.
- EDV
- Aortic Valve opens
- ESV
- Mitral Valve opens
On the Pressure Volume Loop what do the top curve and bottom curve represent?
Top: Contractility
Bottom: Compliance
On the PV Loop
what does the value between
Point 4 and Point 1
represent?
Stroke Volume
On the PVL
what does the top of the curve between Point 2 and 3
represent?
Afterload
What causes
- decreased afterload
- decreased preload
- unchanged SV
- unchanged contractility
Sodium nitroprusside is a short-acting agent that causes balanced vasodilation of the veins and arteries to decrease both left ventricular (LV) preload and afterload.
The balanced vasodilation allows for maintenance of stroke volume and cardiac output at a lower LV pressure (lower cardiac work).
What causes
- decreased afteterload
- increased preload
- Increased SV
- unchanged contractility
An arteriovenous fistula, which can be congenitalor acquired (trauma), allows blood to shunt from the arterial circulation to the venous circulation without passing through the high resistance of the systemic arterioles.
This has the following effects on the LV
What causes
- increased afterload
- Unchanged preload
- increased SV
- Increased Contractility
positive inotrope with minimal vasodilatory/vasoconstrictive effect
(eg, digoxin).
What causes
- increased afterload
- unchanged preload
- decreased SV
- unchanged contractility
Aortic Stenosis
What causes
- Increased Afterload
- Increased Preload
- Increased SV
- Increased Contractility
Exercise
What causes
- Increases afterload
- Increased Preload
- Increased SV
- Unchanged Contractility
IV saline
What causes
- decreased afterload
- decreased preload
- decreased SV
- Unchanged Contractility
Venous Vasodilation
These changes are expected with predominantly venous dilators such as nitrates (eg, nitroglycerin, isosorbide mononitrate, isosorbide dinitrate).
What causes
- Increased Afterload
- Increased Preload
- Decreased SV
- Unchanged Contractility
Vasoconstrictor affecting both the veins and arteries but with no effect on the myocardium (aka contractility)
(eg, the alpha-1 agonist phenylephrine).
On the PV Loop and Starling curve, what causes an:
- Increased (Upward shift) to contractility
- Decreased (Downward shift) to contractility
Increased:
- Myocardial changes with catelcholamines,
- positive ionotropes (Digoxin)
Decreased:
- Loss of functional myocardium (MI),
- Beta Blokers,
- Dilated cardiac myopahty,
- non-DHPR Ca2+ blockers
What are 3 examples that can cause the changes in Ionotropy seen in #1 and 3 examples for changes in #2
1: Catecholamines, digoxin, exercise⊕
2: HF with reduced EF, narcotic overdose, sympathetic inhibition⊝
What are 2 examples that can cause changes in Venous Return/ Blood volume seen in #3 & #4
3: Fluid infusion, sympathetic activity⊕
4; Acute hemorrhage, spinal anesthesia⊝
Intersection of curves = operating point of heart (ie,venous return and CO are equal, as circulatory system is a closed system).
Name one example that can cause the changes of TPR in #5 and 2 examples for changes in #6
5: Vasopressors⊕
6: Exercise, AV-shunt⊝
At What point in the PV Loop is S1 and S2 heard?
Point 1: S1 (Mitral closes)
Point 3: S2 (Aortic Closes)
What causes this curve?
Mitral Regurgitation
Normally, characteristic “V wave” created at the end of passive filling peaks at 10 mmHg.
In MR, an incompetent mitral valve allows backflow of blood from the left ventricle during ventricular systole, leading to markedly elevated left atrial pressure during this time =
early & large V wave peaking at 40 mmHg.
This leads to atrial dilation and often precipitates atrial fibrillation, symptomatically manifesting with palpitations.
What causes this curve?
Aortic Regurgitation
What causes this curve?
Mitral Stenosis
What causes this curve?
Aortic Stenosis
What causes this curve?
Aortic Stenosis
What causes this curve?
Mitral regurgitation
What causes this curve?
Aortic regurgitation
What causes this curve?
Mitral Stenosis
What is this S2 split called?
Physiologic split
Inspiration: Increased delay in P2
What is this S2 split called?
Wide Splitting
What is this S2 split called?
Fixed Splitting
What is this S2 split called?
Paradoxical Split
Seen in conditions that delay RV emptying (eg,pulmonicstenosis, rightbundlebranchblock).
Causes delayed pulmonic sound (especially on inspiration). An exaggeration of normal splitting.
What split?
Wide Splitting
Delayed P2 WIDENS the normally small split between (1st) A2 and (2nd) P2
EX)
Norm: A2 —P2
Wide: A2 ———P2
Heard in ASD.
ASD left-to-right shunt RA and RV volumes flow through pulmonic valve delayed pulmonic valve closure (independent of respiration).
Fixed Splitting
Heard in conditions that delay aortic valve closure
(eg,aortic stenosis, left bundle branch block).
Normal order of semilunar valveclosure is reversed so that P2 sound occurs before delayed A2 sound.
On inspiration, P2 closes later and moves closer to A2, thus eliminating the split.
On expiration, the split can be heard (opposite to physiologic splitting).
Paradoxical split
Norm: I) A2—P2
Norm: E) A2/P2 @ same time
Pdox: E) P2—A2
Pdox: I) A2/P2 @ same time
What causes this curve?
Aortic Stenosis
What causes this curve?
Aortic Stenosis
What causes this curve?
Mitral Regurgitation
*on PV loop, Regurgitation increases SV
&
Stenosis decreases SV
What causes this curve?
Mitral Regurgitation
What causes this curve?
Aortic Regurgitation
What causes this curve?
Aortic Regurgitation
What causes this curve?
Mitral Stenosis
What causes this curve?
Mitral Stenosis
With Time (0-8s) on the X- axis
and
Pressure (0-120 mmHg) on the Y-axis
crudely sketch:
Aortic pressure
LV pressure
LA Pressure
Denote location of:
Systole & Diastole
see attachment
