PCWP and CVP are not good tools for determining ventricular/Blood Volume !
The pulmonary artery catheter is frequently referred to as a Swan-Ganz catheter, in honor of its inventorsJeremy Swan and William Ganz, from Cedars-Sinai Medical Center. The Swan-Ganz balloon flotation catheter was introduced in 1970. It can be placed at the bedside within a few minutes even in critically ill patients. For this purpose it ruled as a gold standard procedure since decades together with misconception .
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The Historical development of the catheter demonstrates that it reached the beside too quickly , without adequate laboratory or clinical research studies . furthermore during those years , no practical guidelines for PA catheter use were agreed on ; therefore misconceptions associated with its use perpetuated .
The catheter’s design and function –as well as its normal limitations, which may vary from patient to patient (ie, position of patient , position of catheter in thorax , with or without positive end-expiratory pressure (PEEP) , and the presence or absence of COPD – were most likely ignored by authors .
Unfortunately , practitioner at many institutions are expose to only a limited number of PA cathertrs annually , and medical residents may only inserts a handful during their 3-years clinical rotation .
These include a lack of ability to recognize waveforms and correlate them to specific hemodynamic conditions ; recognize artifacts or clinical situations in which pulmonary artery occlusion pressure (PAOP) does not accuatetly reflect left ventricular end-diastolic pressure (LVEDP) , such as in mitral valve stenosis .COPD , pneumonectomy , tachycardia , and pulmonary fibrosis .
Another potential source of error is the fact that PA catheters give information on pressure as opposed to volume as set up by the Frank-Staking Law . the conception that PAOP reflects pulmonary venous pressure which in turn is in agreement with left atrial pressure and LVEDP , ins not always the case in critically ill patients . furthermore ,PAOP measurements are useful only when there is a linear relationship between pressure and volume , especially at the end of diastole . the location of the catheter tip so far from the left ventricle can cause readings to be affected by underlying anatomic structures or disease . disorders such as COPD and pulmonary hypertension give falsely elevated PAOP readings and do not permit accurate reflection of actual LVEDP . Pressure changes , directly correlating with ventricular compliance may be affected by several factors such as Myocardial fiber stiffens , temperature , osmolality , and heart rate . Furthermore, PAOP doesn’t take into account pulmonary capillary permeability , interstitial pressure , or actual pulmonary capillary resistance . these factors pla a role in the development of pulmonary edema and therefore affect treatment and management .
Conditions responsible for a discrepancy between PAOP and LVEDP
– Aortic insufficiency
– Pulmonary embolus
– Decreased left ventricular compliance
– Increased intrathoracic pressure
– Non-zone III placement
– Mitral insufficiency
– Mitral valve disese
– Pulmonary vein disorders
Studies shown that, after resuscitation with all shed blood, left ventricular function was markedly impaired as indicated by increased end-Diastolic pressure, decreased aortic pressure , and decreased stroke volume . Systolic contractility was increased, but Diastolic compliance was greatly reduced due to decreased Diastolic maximum and equilibrium volumes they conclude that impaired left ventricular function during hypovolemic shock is due entirely to increased Diastolic stiffness. These results can theoretically be accounted for by a 20% reduction in myocardial muscle length with no change in muscle stress-strain characteristics. This may be the physiological expression of morphologically observed myocardial ‘zonal lesions’ of hypovolemic shock.
Thus, the popular notion that cardiac filling pressures ( the central venous pressure for the right heart , and the pulmonary artery occlusion (wedge) pressure for the left heart ) provide an accurate representation of blood volume status is not supported by experimental studies. There is poor correlation between ventricular filling pressures and ventricular dispensability ( compliance ) on cardiac filling pressures(i.e., a decrease in ventricular dispensability will result in higher cardiac filling pressures at any given ventricular volume ) . In fact, hupovolemia can be accompanied by a decrease in ventricular dispensability (presumably as a result of sympathetic activation ) , which means that cardiac filling pressures will overestimate the intravascular volume status in hypovolemic patients . the cardiac filling pressure can provide qualitative information about the generate stat of intravascular volume , but only when the measurement are very high (e.g.,CVP> 15 mmHg) or very low (e.g.,CVP=0-1 mmHG ) . Intermediated-range measurements are not interpretable.
1- Reliability of clinical monitoring to assess blood volume in critically ill patients . Crit.care Med 1984;12:107-112
2- Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volumes , cardiac performance , or the response to volume infusion in normal subjects .Crit Care med 2004
3- Predicating fluid responsiveness in ICU patients. chest 2002 .
4- Diastolic stiffness impairs left ventricular function during hypovolemic shock in pig . AM J Physio 1991