Part 2A:
*Unique effects of transmural(tm) pressure and intramural(im) pressures*
–Introduction and basic concepts
Some of these ideas are quite convoluted so I’m splitting them up for clarity.
(NB: Some interpretations are a bit personalized so I can’t guarantee accuracy!)
1/
*Unique effects of transmural(tm) pressure and intramural(im) pressures*
–Introduction and basic concepts
Some of these ideas are quite convoluted so I’m splitting them up for clarity.
(NB: Some interpretations are a bit personalized so I can’t guarantee accuracy!)
1/
2/
Definitions:
Consider a hollow organ located in a pressurized compartment.
- The pressure inside the organ = intramural pressure.
- The pressure outside = extramural pressure. -
- The pressure across the wall of the organ is transmural pressure ('mural' = wall).
(See image)
Definitions:
Consider a hollow organ located in a pressurized compartment.
- The pressure inside the organ = intramural pressure.
- The pressure outside = extramural pressure. -
- The pressure across the wall of the organ is transmural pressure ('mural' = wall).
(See image)
3/
*Transmural pressure*
Effect: This is the true distending pressure. As mentioned in the previous thread, LVEDP is an excellent marker of LV preload but the biggest caveat is that it's the transmural pressure that matters.
So what's the extramural pressure of the heart?
*Transmural pressure*
Effect: This is the true distending pressure. As mentioned in the previous thread, LVEDP is an excellent marker of LV preload but the biggest caveat is that it's the transmural pressure that matters.
So what's the extramural pressure of the heart?
4/
The precise answer is pericardial pressure (Pperi). The normal Pperi is negligible (0-1 mmHg). Pperi can be pathologically increased by 2 factors:
(i) Pericardial constraint (including tamponade): more on this in the next thread
(ii) Intrathoracic pressure (ITP) or Ppl:
The precise answer is pericardial pressure (Pperi). The normal Pperi is negligible (0-1 mmHg). Pperi can be pathologically increased by 2 factors:
(i) Pericardial constraint (including tamponade): more on this in the next thread
(ii) Intrathoracic pressure (ITP) or Ppl:
5/
...Any change in ITP is directly transmitted to Pperi. E.g. Tension pneumothorax causes ⬆️⬆️ITP --> ⬆️⬆️ Pperi --> effects similar to tamponade
E.g: Say baseline Pperi = 10 due to pericardial effusion. Then a PTX occurs that raises ITP to 8. Hence, Pperi now becomes 18+8 = 18
...Any change in ITP is directly transmitted to Pperi. E.g. Tension pneumothorax causes ⬆️⬆️ITP --> ⬆️⬆️ Pperi --> effects similar to tamponade
E.g: Say baseline Pperi = 10 due to pericardial effusion. Then a PTX occurs that raises ITP to 8. Hence, Pperi now becomes 18+8 = 18
6/
*Intramural pressure*
We are more intimately familiar with these. Cardiac chamber pressures measured with a catheter (e.g. CVP, PCWP, LVEDP etc.) are all intramural pressures. Therefore, when we use the term ‘PCWP’, we automatically mean ‘imPCWP’.
Effect: Depends on the side.
*Intramural pressure*
We are more intimately familiar with these. Cardiac chamber pressures measured with a catheter (e.g. CVP, PCWP, LVEDP etc.) are all intramural pressures. Therefore, when we use the term ‘PCWP’, we automatically mean ‘imPCWP’.
Effect: Depends on the side.
7/
Intramural pressures on the systemic side affect flow/congestion (left-sided pressures are more complicated – discussed below).
E.g. With high PEEP --> ITP is raised --> ⬆️imCVP --> ⬇️venous return. In other words, imCVP is the actual downstream pressure for venous return.
Intramural pressures on the systemic side affect flow/congestion (left-sided pressures are more complicated – discussed below).
E.g. With high PEEP --> ITP is raised --> ⬆️imCVP --> ⬇️venous return. In other words, imCVP is the actual downstream pressure for venous return.
8/
*Interpreting left-heart pressures: effect of ITP*
When we measure PCWP, we seek to obtain 3 distinct pieces of information:
(a)LV preload - will discuss in a later thread
(b)Tendency for pulmonary venous congestion
(c)Tendency for pulmonary edema
Let's focus on (b) and (c)
*Interpreting left-heart pressures: effect of ITP*
When we measure PCWP, we seek to obtain 3 distinct pieces of information:
(a)LV preload - will discuss in a later thread
(b)Tendency for pulmonary venous congestion
(c)Tendency for pulmonary edema
Let's focus on (b) and (c)
9/
(b)
When we talk about ‘tendency for pulmonary congestion’, we’re basically talking about a high ‘back pressure’ impeding pulmonary venous return, thereby causing sequestration of blood in the pulmonary circulation.
E.g. this may happen in LV failure, MR etc.
(b)
When we talk about ‘tendency for pulmonary congestion’, we’re basically talking about a high ‘back pressure’ impeding pulmonary venous return, thereby causing sequestration of blood in the pulmonary circulation.
E.g. this may happen in LV failure, MR etc.
10/
Key point: Ppl affects the interpretation of PCWP for this purpose.
Any non-zero Ppl will equally affect the heart and the entire pulmonary circulation.
E.g. if Ppl is increased from zero to 10, both pulmonary venous pressure and imPCWP will increase by 10 cmH20... (image)
Key point: Ppl affects the interpretation of PCWP for this purpose.
Any non-zero Ppl will equally affect the heart and the entire pulmonary circulation.
E.g. if Ppl is increased from zero to 10, both pulmonary venous pressure and imPCWP will increase by 10 cmH20... (image)
11/
... Hence, there would be no change in the ‘pressure gradient’ for pulmonary venous return --> no change in ‘tendency for pulmonary congestion’.
Therefore, tmPCWP (imPCWP – Ppl) is the best way to assess ‘tendency for pulmonary congestion’ as it eliminates the effect of Ppl.
... Hence, there would be no change in the ‘pressure gradient’ for pulmonary venous return --> no change in ‘tendency for pulmonary congestion’.
Therefore, tmPCWP (imPCWP – Ppl) is the best way to assess ‘tendency for pulmonary congestion’ as it eliminates the effect of Ppl.
12/
Of note, cardiac pressures are typically measured at end-expiration as Ppl is very close to zero at end-expiration in normal subjects.
Not always true: Obese patients are more likely to have significantly positive Ppl at end-expiration due to mass loading of the chest wall.
Of note, cardiac pressures are typically measured at end-expiration as Ppl is very close to zero at end-expiration in normal subjects.
Not always true: Obese patients are more likely to have significantly positive Ppl at end-expiration due to mass loading of the chest wall.
13/ At our institute, we measure esophageal pressure (Pes) as a surrogate for Ppl to calculate end-exp tmPCWP in these patients.
(c)
‘Tendency for pulmonary edema’ can be assessed by the pressure gradient across the pulmonary capillaries (transmural capillary pressure or tmPc)
(c)
‘Tendency for pulmonary edema’ can be assessed by the pressure gradient across the pulmonary capillaries (transmural capillary pressure or tmPc)
14/
tmPc = imPc – Palv (Palv is the extramural pressure surrounding the pulmonary capillaries).
Although tmPCWP always accurately reflects ‘tendency for pulmonary congestion’, we will later see that it may or may not reflect ‘tendency for pulmonary edema’.
tmPc = imPc – Palv (Palv is the extramural pressure surrounding the pulmonary capillaries).
Although tmPCWP always accurately reflects ‘tendency for pulmonary congestion’, we will later see that it may or may not reflect ‘tendency for pulmonary edema’.
15/
Summary:
- Transmural pressure is the true ‘distending pressure’ and is responsible for wall stress.
- We measure intramural pressures with a catheter.
- Right-sided intramural (measured) pressures affect systemic congestion and flow.
Summary:
- Transmural pressure is the true ‘distending pressure’ and is responsible for wall stress.
- We measure intramural pressures with a catheter.
- Right-sided intramural (measured) pressures affect systemic congestion and flow.
16/
-Left-sided im pressures accurately reflect tendency for pulmonary congestion only when Ppl = 0.
For a non-zero Ppl, tmPCWP is more accurate.
-PCWP (im or tm) may or may not reflect ‘tendency for pulmonary edema’ (later)
-We haven’t even talked about LV preload yet (later!)
-Left-sided im pressures accurately reflect tendency for pulmonary congestion only when Ppl = 0.
For a non-zero Ppl, tmPCWP is more accurate.
-PCWP (im or tm) may or may not reflect ‘tendency for pulmonary edema’ (later)
-We haven’t even talked about LV preload yet (later!)
(For previous/future threads on related topics, follow this original thread - )
P.S. -
