jean robert
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Cardiac physio 3
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| new_n_lost
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D ??
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| unique1
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D
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| silver
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new_n_lost wrote:
D ??
why do you think it's D?
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| new_n_lost
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silver wrote:
why do you think it's D?
I chose it on teh basis of Pulsus paradoxus as it would be clinically present with any restricted filling of the RV.
Ok bear with me and visualise the process....
As the pericardial sac fills with fluid, diastolic filling is increasingly compromised, especially in the low-pressure right ventricle. The right ventricle enlarges which leads to decreased left ventricular filling and therefore reduced Cardiac output. With tamponade, stroke volume decreases, and cardiac output is maintained by an increased heart rate. the Central venous pressure increases and aids diastolic filling. the normal BP is maintained by the physiological changes in the body. As the pericardial pressures increase, the restriction leads to decreased CO which is evidence by hypotenison and thus is a late sequelae of increased pericardial effusion. The first symptom is JVP rising which more of a RVF then a LVF.
Since this is mostly likely chronic development rather than an acute presentation one would expect the adaptations in the musculature of the cardiac muscle and its dynamics.
The only 2 choices which correspond to the setting of a cardiac tamponade are A and D while B and E correlate with LHF and choice C is an acute condition.
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| arlete
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D
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| Jackofknives
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I disagree. Heart failure will only occur if blood supply to the heart is compromised or workload (strain) is too high, which shouldn’t be the case bc hypertension is absent and venous return is not going to be markedly elevated secondary to tamponade.
This is constrictive heart disease, stroke volume falls due to fall in preload and the body maintains blood pressure by increasing heart rate. How do you do that? By increasing sympathetic activity and decreasing parasympathetic output to the heart. The vasomotor center in the brain stem will have spillover affect on the respiratory center and cause hyperventilation. In addition, as the question indicates, because the left ventricle is considerably thicker than the right, the left ventricular chamber is more vulnerable to restrictions, causing a difference in cardiac output between the two chambers, in which the output of the right ventricle is greater than the left simply because of greater preload. This in turn causes pulmonary hypertension and pulmonary edema.
So my answer is E.
PS.
Anxiety is due to sympathetic overload. Difficulty breathing could be the result of lung cancer or pulmonary edema. Systemic vein distention indicates congestion of the right ventricle, this in turn can lead to right ventricular failure but it is a long process and cannot be the initially effect.
Edited by Jackofknives on 12/25/07 - 04:40 PM
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| arlete
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 Because the RIGHT ventricle is considerably thinner than the left, the RIGHT ventricular chamber is more vulnerable to restrictions. This leads to right ventricular failure, acutely, and JVD. The blood does not reach the lungs (therefore, patient has SOB) and left ventricle. If you listen, the lungs are clear, there's no congestion there.
The only situation where the right ventricle output will congest the lungs is when you have a left to right shunt, that chronically leads to pulmonary hypertension. Acutely, it's the LEFT ventricle failure that leads to pulmonary congestion. Right ventricle problems lead to venous congestion.
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| new_n_lost
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Jackofknives wrote:
I disagree. Heart failure will only occur if blood supply to the heart is compromised or workload (strain) is too high, which shouldn’t be the case bc hypertension is absent and venous return is not going to be markedly elevated secondary to tamponade.
This is constrictive heart disease, stroke volume falls due to fall in preload and the body maintains blood pressure by increasing heart rate. How do you do that? By increasing sympathetic activity and decreasing parasympathetic output to the heart. The vasomotor center in the brain stem will have spillover affect on the respiratory center and cause hyperventilation. In addition, as the question indicates, because the left ventricle is considerably thicker than the right, the left ventricular chamber is more vulnerable to restrictions, causing a difference in cardiac output between the two chambers, in which the output of the right ventricle is greater than the left simply because of greater preload. This in turn causes pulmonary hypertension and pulmonary edema.
So my answer is E.
PS.
Anxiety is due to sympathetic overload. Difficulty breathing could be the result of lung cancer or pulmonary edema. Systemic vein distention indicates congestion of the right ventricle, this in turn can lead to right ventricular failure but it is a long process and cannot be the initially effect.
1. How does the LV failure before the RV failure occur in the setting of a Tamponade.
2. The question doesnt indicate in any way that the left ventricle is enlarged it simply states that there is a difference in size of the ventricles.
3. Why is there Raised JVP in your setting of scenario. Correct me if i m wrong that JVP only rises when there is RV failure due to any cause.
Secondly According to Goljan pg 192 point 3 of pericardial effusion JVP is due to the non entry of blood in the Rt Atrium.
More objections coming brb 
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| SmokyWaters
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I think its HYPOTENSION
ITS A PART OF BECK'S TRIAD
RIGHT VENTRICLE NOT FILLING UP... AS CONNECTED IN SERIES WONT LET LEFT VENTRICLE FILL UP
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| Jackofknives
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Come on man, use your imagination, im exaggerating a bit, but if you had a chamber with huge walls and a tiny little room, and you have another chamber with a huge room and a wall thin as paper, which chamber do you think would care more if you decided to reduce the size of its room. Ofc the one with the thicker wall, because its room is already small enough. I cant explain it better than this, so if you still dont get it then consult your anatomy atlas or something.
Let me give you an example.
Since we all agree on that the left ventricular chamber is more compressed, its diastolic volume is reduced to a greater extent than the right ventricle. What does that mean? Well, according to Starling’s law, venous return equals cardiac output, or simply put what comes in – get outs. Since the right ventricular chamber can room slightly more blood than the left you have this situation –
Right ventricle ejects 100 ml per stroke; left ventricle ejects 99 ml per stroke. If this happen acutely, lymphatic drainage does not yet have time to compensate in term of increased suction and you have 1ml x 60 stroke per minute = 60 ml blood accumulate in the lung every minute. What does that lead to? Pulmonary edema. How long does that take? A couple of minutes, the patient will die within half an hour due to suffocation. Note, in the none constricted heart, this is not a problem, because this would lead to greater preload to the left ventricle which would cause it to increase its ejection volume, however this compensation cannot take place because of the pericardial restriction.
When does right ventricle fail? When the pulmonary pressure increases far enough that it greatly reduces the cardiac output of the right ventricle, analogous to the situation in which systemic hypertension causes left ventricular failure, because more work is needed to eject blood against the pressure gradient. How long does that take? Days.
Why is there systemic vein distention? First you have to get the concept right, the aetiology is that right atrial pressure increases from its normal value of –4 mm Hg to above 0 mm Hg. Now systemic vein pressure also increase from 0 mm Hg to even 10 mm Hg or slightly more to cope with this. However, the compensation is not good enough and pressure gradient between systemic veins and right atrium is diminished secondary to increased right ventricular pressure and as a result blood stasis is seen in the veins. However, again, this is secondary to elevated pulmonary pressure, nowhere does it say that systemic vein distention is going to be the first sign that you see and the question is which sign do you see FIRST.
Edited by Jackofknives on 12/26/07 - 12:30 AM
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| arlete
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I didn't agree the left ventricle is more compressed! I think that is the basic concept you are getting wrong, and all your thinking goes wrong from that on. If you ever see an echo of a patient with cardiac tamponade, you'll have it all straightened up, for sure... All the physiopathology starts by the right ventricle being squeezed. The thick muscular left ventricle is less susceptible to external forces.
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| SmokyWaters
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A :$
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| arlete
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Actually, at the echo, the right atrium is the chamber that suffers the most with cardiac tamponade... 
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| jean robert
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new_n_lost wrote:
D ??
Correct answer: D
Here is the explanation
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| new_n_lost
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arlete wrote:
I didn't agree the left ventricle is more compressed! I think that is the basic concept you are getting wrong, and all your thinking goes wrong from that on. If you ever see an echo of a patient with cardiac tamponade, you'll have it all straightened up, for sure... All the physiopathology starts by the right ventricle being squeezed. The thick muscular left ventricle is less susceptible to external forces.
And neither did i. Though i agree with Arlete on where your concepts get sidetracked.
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| arlete
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