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CENTRAL VENOUS PRESSURE AND PEEP


“Central venous pressure measurement is not a surrogate of intravascular volume or ventricular preload for fluid resuscitation. For this, fluid responsiveness has to be assessed.”
This discussion is for physiological purpose only.

Invasive pressure monitoring of central venous pressure, is measurement of intramural pressure (Pim) of the vessel.        

                                                    

                               
Flow across a vessel is a function of intramural pressure gradient and resistance to the flow.
                                    Force driving flow (F) = ∆P/ R

                                                     

According to Poiseuille equation resistance is inversely proportional to fourth power of radius.
                                                     
                         (ⁿ= viscosity of fluid, L= length of tube, r= radius of tube)

Radius of a distensible tube depends on transmural pressure (Ptm), which is the difference between intramural pressure and surrounding pressure (Psur).

                                                               Ptm = Pim – Psur

                                                      
                                     
Surrounding pressure for intrathoracic vascular structure is intrathoracic pressure, which is pleural pressure (Ppl).

In a collapsible tube, if volume is not allowed to change, then change in surrounding pressure (Psur) will bring about similar change in intramural pressure (Pim), so that transmural pressure (Ptm) remains unchanged. As volume will remain unchanged only if transmural pressure remains constant.

                                                      
                                       
Thus in positive pressure ventilation changes in pleural pressure will bring about similar change in intramural pressure of central vein, and this intramural pressure is measured as central venous pressure.

Pleura space is a potential space between lung and chest wall, lined by visceral and parietal pleura respectively. Pleural pressure is a function of elastance/ compliance of lung and chest wall, which act in opposite direction.

Compliance and elastance are inverse of each other.

In positive pressure ventilation, relationship between applied airway pressure (PEEP) and pleural pressure is dependent upon the compliance/ elastance of the lung and chest wall.

If lung compliance is low, the end expiratory lung volume (EELV) achieved by applied airway pressure (PEEP will also be low and therefore the change in pleural pressure will also be low.

So, worse the lung compliance and greater the chest wall compliance, lower will be the change in pleural pressure for an applied airway pressure (PEEP). Therefore stiff lungs with good chest wall compliance (ARDS/ ILD lung in a thin individual) will have minimal change in pleural pressure with increasing airway pressure.

On the other hand, in patients with normal compliant lung with stiff chest wall (obese or abdominal compartment syndrome), pleural pressure will change markedly with applied airway pressure (PEEP).

Now let us calculate the changes in pleural pressure with applied airway pressure.

A young, thin patient with ARDS is being ventilated with a PEEP of 16 cmH2O.  In this patient lung compliance is 30 ml/ cmH2O (markedly decreased) and chest wall compliance is 100 ml/ cmH2O(normal).

At end expiration the lung volume (end expiratory lung volume- EELV) will be 480 ml.

                                    EELV = Applied pressure (PEEP) × Lung Compliance

                                    EELV = 16 × 30 = 480 ml

Resulting pleural pressure will be the pressure applied by this lung volume in overcoming the elastance of chest wall.

                                Plerual pressure = EELV / Chest wall Compliance

                                Pleural pressure = 480 / 100 = 4.8 cmH2O = 3.5 mmHg.

Thus if measured CVP is 18 mmHG, real CVP will be 15.5 mmHg (18-3.5), an insignificant difference.

Now let us consider an young, obese patient with pulmonary hypertension, ventilated with a PEEP of 10 cmH2O. In this patient lung compliance is normal (100 ml/ cmH2O) but chest wall compliance is low (60 ml/cmH2O) because of obesity.

With similar calculation the EELV will be 1000 ml and pleural pressure will be 16 cmH2O (12 mmHg).

If measured CVP is 16 mmHg, real CVP will be 4 mmHg (16-12), a very significant difference.

Therefore changes in CVP, brought about by applied PEEP is a function of relative compliance of the lung and chest wall.

Stiff lung ventilated with high PEEP, will not result in significant alteration in measured CVP.

Whereas stiff chest wall with normal lung, ventilated with high PEEP, will result in marked change in measured CVP.

High PEEP is needed in stiff lung, stiff chest wall (obesity or abdominal compartment syndrome) and cardiogenic shock (to reduce afterload).

Comments

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