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Cardiac values

normal indicies and drug review

CO: vol/min
CO= 4-8 L/min
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= 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
Created by: scofor