Coronary perfusion pressures

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

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. 

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]. 

Isoprenaline stimulates pi and 32 adrenoceptors (pi>32) resulting in increased myocardial contractility and reduced peripheral vascular resistance. It does not act on a adrenoceptors. Cardiac output increases partly due to reduced afterload and an increase in heart rate. There is a diversion of blood to non-essential tissues, e.g. skeletal muscle and skin. Because of the decrease in peripheral vascular resistance arterial blood pressure and coronary perfusion pressure may decrease, which may predispose to myocardial ischaemia. 

Pretreatment with G115 reduces by 30% coronary perfusion pressure... 

Langendorff-perfused rat heart have been investigated and compared to that of nifedipine. Nifedipine decreased concentration-dependent (IC50 = 8.89 1.09 x 10-8 M) left ventricular pressure leaving unaltered coronary perfusion pressure, whereas DP7 did not affect these parameters. Nifedipine did not modify QRS and QT intervals of ECG [112], It has also been investigated that neither pyruvate kinase nor lactate dehydrogenase was inhibited by DP7... 

Hearts from CD-I male rats (250-300 g n=4 each group, 34 total) are excised and perfused within 25 s to 2 min with non-recirculating oxygenated Krebs-Henseleit bicarbonate buffer (120 mM NaCl, 25 mM NaHCOj, 1.2 mM MgSO -ZHp, 5 mM KCl, 1.7 mM CaCl-2H20, 10 mM glucose, pH 7.4, 37°C) at a constant coronary perfusion pressure (CPP) of 80 mm Hg (18, 19). 

Global ischemia (25 min) is initiated by decreasing the coronary perfusion pressure (CPP) to zero within 60 s (see Note 1). 

Perfuse heart during normoxia at a coronary perfusion pressure of 80 mmHg. 

After 25 min of no-flow ischemia, reperfuse the heart for 30 min at a coronary perfusion pressure of 80 mmHg (see Note 8). 

To avoid collapse of coronary arteries, decrease coronary perfusion pressure gradually over a 60 s period from 80 mmHg to 0 mmHg. 

To avoid damages to coronary arteries, increase coronary perfusion pressure gradually over a 15 s period from 0 mmHg to 80 mmHg. 

Paradis NA, Martin GB, Rivers EP, et al. Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. JAMA 1990 263 1106-1113. 

Cardiovascular Cardiovascular stability after induction is a major advantage of etomidate over either barbiturates or propofol. Induction doses of etomidate typically produce a small increase in heart rate and little or no decrease in blood pressure or cardiac output. Etomidate has little effect on coronary perfusion pressure while reducing myocardial consumption. Thus, of all induction agents, etomidate is best suited to maintain cardiovascular stability in patients with coronary artery disease, cardiomyopathy, cerebral vascular disease, or hypovolemia. 

Critical coronary perfusion pressure. As stated above, flow is related to the pressure gradient. However, in stenotic vessels, flow will remain disproportionaUy low, as autoregulation cannot cause the maximal vasodilation in the healthier vessels. This may exacerbate regional hypoxia, the build up... 

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