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Hemodynamic Monitoring

Updated: Mar 22



Cardiac Output (CO) = heart rate (HR) x stroke volume (SV) – the amount of blood ejected by left ventricle per contraction.


o As heart rate increases, CO increases to a point. Extreme tachycardia will decrease CO since diastolic filling time is reduced.

o Extreme bradycardia results in low CO and hypotension.

o Normal CO is 4-8 L per minute

o Normal CI is 2.5-4.0 L/min/M2 – takes body surface area into account and is more meaningful than CO.


Stroke volume (SV) is how many mLs per beat the left ventricle ejects.


o Normal SV = 50-100 mL per beat

o SV is influenced by contractility of the ventricles, preload (volume/pressure), and afterload (resistance).

o Frank-Starling’s Law –heart stretches with volume to increase contractility (think rubber band).


Preload is the volume/pressure in the ventricle at end diastole after the AV valves close.


o Right atrial pressure (RAP)/central venous pressure (CVP) = right ventricular preload

o Pulmonary artery occlusive pressure PAOP – left ventricular preload

o As preload increases, SV and CO increase to a point.

o Preload is decreased in hypovolemia and from vasodilators. Treat with volume expanders and vasopressors.

o Preload is increased by increased volume (leads to heart failure) and vasoconstrictors Treat with diuretics and vasodilators like Nitrates and Morphine.


Afterload is the pressure/resistance to ventricular emptying.


o As afterload increases, SV and CO increase.

o Pulmonary vascular resistance (PVR) = right ventricular afterload (pulmonic).

o Systemic vascular resistance (SVR) = left ventricular afterload (aortic).

o Decreased in distributive shocks (neurogenic, septic, and anaphylactic) and by vasodilators. Treat with Norepinephrine, Phenylephrine, Epinephrine.

o Increased in hypertension, aortic stenosis, vasopressors, and through shock compensation (decreases stroke volume and CO). Treat with Nitroprusside, ACE inhibitors (prils), calcium-channel blockers (CCB), Nitrates, IABP.


Contractility is the contractile force of the myofibrils.


o As contractility increases, SV and CO increase. Increase contractility with positive inotropes like Dobutamine, Dopamine. Decrease contractility with negative inotropes like beta-blockers (olols) and CCBs.



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