Dr. Jared Robl, PGY-2
April 27th, 2021
* Mean Arterial Pressure = Cardiac Output x Systemic Vascular Resistance
* Cardiac Output (L/min) = heart rate (bpm) x SV (ml)
* Determinants of Stroke Volume are
o 1) Preload
* the end diastolic volume (not the EDP! though these two are correlated)
* this length tension relationship is described classically as the Frank Starling mechanism
* LV preload = LVEDP = LAP = PCWP
* RV preload = CVP
o 2) Afterload
* is not simply the aortic or systolic blood pressure (though that does certainly contribute); rather afterload is best thought of as the ventricular wall stress during systole, which is described by the law of Laplace as follows:
* Wall Stress = LV transmural pressure x LV radius / 2 x wall thickness
o where LV transmural pressure = intraventricular pressure – pericardial pressure
* this concept explains tons of cardiovascular physiology
* i.e. why diuresis decreases afterload in addition to preload (via decreasing the LV radius)
* i.e. why positive pressure ventilation decreases both preload and afterload (the latter via increasing pericardial pressure and therefore decreasing LV transmural pressure)
o 3) Contractility
* AKA inotropism: under a given set of loading conditions (that is to say fixed preload & afterload) how much tension can the myocyte sarcomeres generate
* Pulse Pressure = systolic blood pressure – diastolic blood pressure
* how can we measure cardiac output with a Swan Ganz catheter?
o Fick’s Method
* takes into account that your body extracts oxygen from the blood as it flows: Oxygen Consumption (VO2) = Cardiac Output (Q) x avO2 difference
* rearranged: Q = VO2 / avO2
* we estimate VO2 with a nomogram, and can measure SaO2 & SvO2; can therefore derive Q
o Thermodilution Method
* by introducing saline at a known temperature and then reassessing the temperature downstream at a certain time interval, you can back calculate flow; this is reliant however on the assumption of completely forward flow (no valvular regurgitation or shunt); thus not very accurate in reality
* Venous Oximetry
o SvO2 implies true “maximally mixed” pulmonary artery blood; whereas ScvO2 is collected from the SVC
o SvO2 is a product of the oxygen delivered to the tissues minus the oxygen extracted by the tissues
o under normal conditions SvO2 is ~ 75%, meaning your body extracts ~ 25% of O2 from the arterial blood
o a low SvO2 can be indicative of cardiogenic shock, whereas high SvO2 favors distributive
o always interpret SvO2 in the setting of the [hemoglobin], arterial oxygen saturation, and metabolic demand of the tissue
* heart failure = inability of heart to meet body’s metabolic demands at physiologic normal filling pressures
* cardiogenic shock = any cardiac mediated condition that results in circulatory dysfunction with end organ hypoperfusion
* the ESCAPE trial in 2005 showed no benefit of routine Swan placement, this means that you should only use if there is diagnostic uncertainty or it’s changing your management, otherwise simply incurring risk w/o benefit
* treatment of cardiogenic shock entails correcting any reversible cause and then the optimization of preload, afterload, and contractility. If not enough then consider mechanical support.
* IABPs are unique devices in that they lower afterload (via vacuum effect) & augment coronary blood flow all without reducing MAP, no medicine can do this. However, the IABP-SHOCKII trial showed no mortality benefit.
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