Cardiac Physiology...• Cardiac Output = Increases Increases Perception: fluid increases PRA leading to an augmentation of CO through the Frank-Starling mechanism. \爀屲1\⤀ 䤀渀挀爀攀愀猀攀
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Cardiac Physiology William G. McMaster, Jr. Bonus Conference, 6/19/2013 A Very Brief But Hopefully Helpful Lecture
William G. McMaster, Jr. Bonus Conference, 6/19/2013
A Very Brief
But Hopefully Helpful Lecture
Basic Physics
• Poiseuille’s Law:
– Q (flow)=P/R – Flow is proportional to pressure and inversely
proportional to resistance
Presenter
Presentation Notes
Heart Rate (HR): Number of heart beats per minute Stroke Volume (SV): Volume of blood ejected by the left ventricle per beat 60 to100 cc /beat Cardiac Output (CO): Volume of blood ejected by the left ventricle per minute CO = HR x SV 4 to 8 L/min Systemic Systolic Pressure (SP): The highest pressure in the aorta after blood is ejected Systemic Diastolic Pressure (DP): The lowest pressure in the aorta after blood is ejected Systemic Pulse Pressure: SP minus DP Systemic Mean Arterial Pressure (MAP): Equals DP+(SP-DP)/3 or (2xDP + SP)/3 Equals (CO x SVR) + CVP 70 to 100 mmHg Central Venous Pressure (CVP): The pressure at which the right atrium (and the right ventricle) is filling Right Ventricular End Diastolic Pressure: pressure inside the RV at the end of diastole Pulmonary Artery Systolic Pressure (PAS): The highest pressure in the pulmonary artery after blood is ejected Pulmonary artery Diastolic Pressure (PAD): The lowest pressure in the pulmonary artery after blood is ejected Pulmonary Capillary Wedge Pressure (PCWP): The pressure at which the left atrium (and the left ventricle) is filling Systemic Vascular Resistance (SVR): The resistance that blood has to overcome in order to flow thru the different body organs 800 to 1200 dynes-sec/cm5 Pulmonary Vascular Resistance (PVR): The resistance that blood has to overcome in order to flow thru the pulmonary circulation 50 to 250 dynes-sec/cm5
Perception: fluid increases PRA leading to an augmentation of CO through the Frank-Starling mechanism. 1) Increase in mean systemic pressure by increasing blood volume (increases venous return and CO) 2) Decreased resistance 2/2 hemodilution 3) Decreased viscosity decreases pulmonary arterial afterload For the most part, a fluid bolus increases VR by increasing Pms and causing an increase in flow to the right heart, thereby taking advantage of the Frank-Starling mechanism to increase CO. However, this parallel shift in the VR curve does not fully account for the increased CO when crystalloid is infused
phenylephrine and vasopressin With the addition of a pure vasoconstrictor, the net effect is a decrease in VR/CO but with an increase in the measured PRA. Increase resistance (decreased VR slope without a change in Pms) as a consequence of vasoconstriction of large veins and the vena cava pure vasopressors also constrict venules and small veins and this increases the relative proportion of Vs to Vo. This will increase Pms and tend to offset some of the decrease in VR (shifting the VR intercept with the abscissa [Pms] to the right Pure vasoconstrictors also usually generate an increased ventricular afterload (shifting the ventricular function curve downward; Fig. 7, point C to D). This again tends to decrease VR/CO. In summary, the net clinical effect of pure vasopressor administration is usually a decrease in VR/CO with an increase in PRA and related filling pressures.
Inodilators like dobutamine and milrinone generate distinctly different hemodynamic effects. primary effect: venodilatation of both capacitance and resistive elements of the venous circuit. Rv falls and the slope of the VR relationship becomes steeper (Fig. 8, point A to B), which tends to drive up VR. However, this effect is partially offset by a decrease in the proportion of Vs to Vo, which reduces Pms (Fig. 8, point B to C). The combination of arteriolar vasodilator activity and direct myocardial inotropic effect results in a marked increase in effective contractility and a shift of the ventricular function relationship upward (Fig. 8, point C to D). The effect is a substantial increase in Venous Return / Cardiac Output with a concomitant decrease in Right Aterial Pressure and related filling pressures.
Dobutamine
• Pure Inotrope • Starting dose: 2mcg/kg/min
Milrinone • Positive inotrope and Vasodilator
• Decreases SVR and PVR • Used mainly in the setting of RV dysfunction • Starting dose: 3.75 mcg/kg/min
Inotropic Vasopressors
Effect: • Venous Return / Cardiac Output = • RA pressures and related filling pressures are typically
unchanged or modestly increased
Increases
Presenter
Presentation Notes
Vasopressors with inotropic activity such as dopamine and norepinephrine have effects that are intermediate between pure vasopressors and inodilators. Increase afterload, decrease CO Increase PMS, increase VR, increased CO Inotropic effects are not as great 2/2 increased afterload 1) α-1 adrenergic agonist activity generates significant vasoconstriction resulting in a shallower VR response curve (Fig. 9, point A to B) 2) the capacitance beds are also constricted resulting in a shift of venous volume toward Vs, which shifts Pms to the right (Fig. 9, point B to C). 3) Because direct myocardial inotropic effects are partially offset by arteriolar vasoconstrictor effects (which increases ventricular afterload), the right ventricular cardiac function curve is not as markedly shifted as seen with the inodilator group (Fig. 9, point C to D). The net effect of a vasopressor with inotropic activity is generally to increase VR/CO, although not to the extent seen with inodilators. In addition, PRA and related filling pressures are typically unchanged or modestly increased (at small to moderate drug doses).
Perception: fluid increases PRA leading to an augmentation of CO through the Frank-Starling mechanism. 1) Increase in mean systemic pressure by increasing blood volume (increases venous return and CO) 2) Decreased resistance 2/2 hemodilution 3) Decreased viscosity decreases pulmonary arterial afterload For the most part, a fluid bolus increases VR by increasing Pms and causing an increase in flow to the right heart, thereby taking advantage of the Frank-Starling mechanism to increase CO. However, this parallel shift in the VR curve does not fully account for the increased CO when crystalloid is infused
Presenter
Presentation Notes
phenylephrine and vasopressin With the addition of a pure vasoconstrictor, the net effect is a decrease in VR/CO but with an increase in the measured PRA. Increase resistance (decreased VR slope without a change in Pms) as a consequence of vasoconstriction of large veins and the vena cava pure vasopressors also constrict venules and small veins and this increases the relative proportion of Vs to Vo. This will increase Pms and tend to offset some of the decrease in VR (shifting the VR intercept with the abscissa [Pms] to the right Pure vasoconstrictors also usually generate an increased ventricular afterload (shifting the ventricular function curve downward; Fig. 7, point C to D). This again tends to decrease VR/CO. In summary, the net clinical effect of pure vasopressor administration is usually a decrease in VR/CO with an increase in PRA and related filling pressures.
Presenter
Presentation Notes
Inodilators like dobutamine and milrinone generate distinctly different hemodynamic effects. primary effect: venodilatation of both capacitance and resistive elements of the venous circuit. Rv falls and the slope of the VR relationship becomes steeper (Fig. 8, point A to B), which tends to drive up VR. However, this effect is partially offset by a decrease in the proportion of Vs to Vo, which reduces Pms (Fig. 8, point B to C). The combination of arteriolar vasodilator activity and direct myocardial inotropic effect results in a marked increase in effective contractility and a shift of the ventricular function relationship upward (Fig. 8, point C to D). The effect is a substantial increase in Venous Return / Cardiac Output with a concomitant decrease in Right Aterial Pressure and related filling pressures. pressures.
Presenter
Presentation Notes
Vasopressors with inotropic activity such as dopamine and norepinephrine have effects that are intermediate between pure vasopressors and inodilators. Increase afterload, decrease CO Increase PMS, increase VR, increased CO Inotropic effects are not as great 2/2 increased afterload 1) α-1 adrenergic agonist activity generates significant vasoconstriction resulting in a shallower VR response curve (Fig. 9, point A to B) 2) the capacitance beds are also constricted resulting in a shift of venous volume toward Vs, which shifts Pms to the right (Fig. 9, point B to C). 3) Because direct myocardial inotropic effects are partially offset by arteriolar vasoconstrictor effects (which increases ventricular afterload), the right ventricular cardiac function curve is not as markedly shifted as seen with the inodilator group (Fig. 9, point C to D). The net effect of a vasopressor with inotropic activity is generally to increase VR/CO, although not to the extent seen with inodilators. In addition, PRA and related filling pressures are typically unchanged or modestly increased (at small to moderate drug doses). ).
Ejection Fraction EF is a measurement of the heart’s efficiency
• EF >55%, then the LV function is normal • <55% but >30%, then the LV function is moderately
depressed • <30%, then the LV function is severely depressed
Presenter
Presentation Notes
EF is a measurement of the heart’s efficiency EF is equal to the amount of blood pumped divided by the amount of blood in the LV prior to contraction, at the end of diastole i.e.: LVEDV If EF >55%, then the LV function is normal If EF<55% but >30%, then the LV function is moderately depressed If EF<30%, then the LV function is severely depressed
