normal indicies and drug review

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CO:  vol/min  
CO=  4-8 L/min  
CI:  CO/BSA  
CI=  2.5-5.0 L/min/m2  
MAP:  [LVP + 2 (RAP)]/3  
MAP=  80-100 mmHg  
MPAP:  [RVP + 2 (LAP)]/3  
MPAP=  10-20 mmHg  
UO=  60 mL/hr  
CVP:  RAP, reflecting total vol.  
CVP=  2-6 mmHg  
PCWP:  LAP=LVEDP  
PCWP=  4-12 mmHg  
SVR:  [(MAP-CVP)*80]/CO  
SVR=  900-1400 dynes x s x cm5-  
PVR:  { (PAP-CVP)* 80 } / (CO)  
PVR=  150-250 dynes x s x cm-5  
MC RMP=  -80 to -90 mV  
affect of inhibiting Na+ influx into MC:  Phase 0 less steap/high, increased refractory time, decreased HR  
Phase of MC AP involving Mg:  Phase 4 for function of NaK pump restoring ion balence  
SA node rate=  60-100  
AV junction rate=  40-60  
Ventricle rate=  <40  
Absolute Refract:  P to mid T  
Relative refract:  Mid to end T  
Intropin 1-2 ug/kg/min:  promote renal, mesenteric blood flow? not  
Intropin 2-10 ug/kg/min:  inotropic effects  
Intropin >10 ug/kg/min:  vasopressor (constriction)  
Dig FX  +contractility, -dromotropic  
treat PACs:  verapamil, diltiazem  
treat Afib/flut:  Ca++/B/Dig,Procainamide  
treat SVT/PSVT:  adenosine, Ca/B/K block  
treat Vtach/fib:  Epi/vasopressin, lidocaine, amiodorone, MgSO4, procain  
I AA mechanism:  block influx of Na into both MC (phase 0) and PM cell (phase 4)... - conductivity and + refractory time; - automaticity (- HR)  
II AA mechanism:  Block the B1 receptors  
III AA mechanism:  slow efflux of K+ out MC, so repolarization +; +absolute refractory time; -conduction; -automaticity (- K out of cell, -phase 4 steepness  
IV mechanism:  -Ca influx (-HR), prevents SM contraction, vascular relaxation  
adenosine mechanism:  stimA1,-AV cond,-HR, +vasoD  
MgSO4 mechanism:  return ion balence esp. during CPR  
treat acute HT  Nipride  
treat + precap arteriole R  Nipride, Adalat, Capoten, Vasotec  
treat + precap venule R  Morphine  
Persantine FX  (dypyrimidamole) inhibits platelet aggregation  
Cardiazem FX  (diltiazem) -Mi02, -HR, vasoD  


   

 
 

 
 

 

 
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