Perfusion pressure

FIGURE 9.14 Effects of adenosine receptor agonist 2-chloro-adenosine on vascular perfusion pressure of isolated perfused rat kidneys. Minor effects seen in untreated kidneys (filled circles) and pronounced vasoconstriction while vasodilatation in kidneys coperfused with subthreshold concentrations of a-adrenoceptor vasoconstrictor methoxamine and vasodilatatory activation of adenylyl cyclase with forskolin (open circles). Redrawn from [49]. 

Perifascicular capillaries are closer to aggregates of antibody-secreting cells (B-lymphocytes) situated in perimysial connective tissue and therefore are most severely affected by antibody-dependent cytotoxic reactions. Immune-complex deposition occurs at a higher level in the vascular tree (i.e., at arteriolar level) and this may cause fluctuations in perfusion pressure. Perifascicular capillaries are most distal from the head of vascular pressure and therefore most likely to suffer from periodic anoxia. 

Georgiadis D, Schwarz S, Kollmar R, Baumgartner RW, Schwab S. Influence of inspiration expiration ratio on intracranial and cerebral perfusion pressure in acute stroke patients. Intensive Care Med 2002 28(8) 1089-1093. 

Rosner MJ, Coley IB. Cerebral perfusion pressure, intracranial pressure, and head elevation. J Neurosurg 1986 65(5) 636-641. 

Fan JY. Effect of backrest position on intracranial pressure and cerebral perfusion pressure in individuals with brain injury a systematic review. J Neurosci Nurs 2004 36(5) 278-288. 

Meixensberger J, Baunach S, Amschler J, Dings J, Roosen K. Influence of body position on tissue-po2> cerebral perfusion pressure and intracranial pressure in patients with acute brain injury. Neurol Res 1997 19(3) 249-253. 

Chan K-H, Miller JD, Dearden NM, Andrews PJ, Midgley S. The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury. J Neurosurg 1992 77(1) 55-61. 

Maintain cerebral perfusion pressure (CPP) between 60-80 mmHg... 

S. Fujita, D.L. Roerig, Z.J. Bosnjak, and D.F. Stowe, Effects of vasodilators and perfusion pressure on coronary flow and simultaneous release of nitric oxide from guinea pig isolated hearts. Cardiovasc. Res. 38, 655-667 (1998). 

The goal of sympathomimetic therapy is to augment both coronary and cerebral perfusion pressures during the low-flow state associated with CPR. These agents increase systemic arteriolar vasoconstriction, thereby improving coronary and cerebral perfusion pressure. They also maintain vascular tone, decrease arteriolar collapse, and shunt blood to the heart and brain. 

Coronary perfusion pressure should be assessed in patients for whom intraarterial monitoring is in place. 

Kidneys are exquisitely sensitive to changes in perfusion pressures. Moderate alterations can lead to significant changes in glomerular filtration rate. Oliguria, progressing to anuria, occurs because of vasoconstriction of afferent arterioles. 

Successful fluid resuscitation should increase SBP (greater than 90 mm Hg), Cl (greater than 2.2 L/min/m2), and urine output (0.5 to 1 mL/kg/hour) while decreasing SVR to the normal range. MAP greater than 60 mm Hg should be achieved to ensure adequate cerebral and coronary perfusion pressure. 

CPP is coronary perfusion pressure and ADP is aortic diastolic pressure. 

The ability of an organ to regulate its blood flow despite changes in its perfusion pressure. 

Nordstrom CH. 2003. Assessment of critical thresholds for cerebral perfusion pressure performing bedside monitoring of cerebral energy metabolism. Neurosurg Focus... 

Nordstrom CH, Reinstrup P, Xu W, Gardenfors A, Ungerstedt U. 2003. Assessment of the lower limit for cerebral perfusion pressure in severe head injuries by bedside monitoring of regional energy metabolism. Anesthesiology 98(4) 809-814. 

Stahl N, Ungerstedt U, Nordstrom CH. 2001b. Brain energy metabolism during controlled reduction of cerebral perfusion pressure in severe head injuries. Intensive Care Med 27(7) 1215-1223. 

Since Kantrovitz et al. described the concept of counterpulsation in 1968 [3], the lABP has been the mainstay for temporarily augmenting the cardiac output and improving hemodynamics in acutely decompensated refractory HF [4, 5]. lABP use has been shown to reduce heart rate, left ventricular end-diastolic pressure, mean left atrial pressure, afterload, and myocardial oxygen consumption by at least 20-30%. The lABP also modestly increases coronary perfusion pressure and decreases the right atrial pressure, pulmonary artery pressure, and pulmonary vascular resistance [6]. 

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