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Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
Normal cardiac output: 4–8 liters per minute in an adult at rest. Cardiac index (CI) normalizes CO for body surface area: CI = CO / BSA. Normal CI: 2.2–4.0 L/min/m². A CI below 2.2 in the clinical context suggests low output; below 1.8 is cardiogenic shock territory.
Stroke volume is the amount of blood ejected per heartbeat (normally 60–100 mL). Stroke volume is determined by three variables: preload, afterload, and contractility.
Definition: Preload is the degree of stretch of the ventricular myocardial fibers at end-diastole — essentially, how full the ventricle is just before it contracts. The Frank-Starling law states that within physiological limits, increased preload (more stretch) produces increased stroke volume (a stronger contraction). The heart pumps more when it is filled more — up to a point. Beyond that point (ventricular overdistension), further preload increases don't improve and can decrease stroke volume.
Clinical correlates of preload: Right ventricular preload is estimated by central venous pressure (CVP) — normal 2–8 mmHg. Left ventricular preload is estimated by pulmonary capillary wedge pressure (PCWP) via PA catheter — normal 6–12 mmHg. These static measures have significant limitations; dynamic measures (pulse pressure variation, straight leg raise response) are more reliable indicators of preload responsiveness in mechanically ventilated patients.
How to optimize preload: Low preload (volume-depleted, dehydrated, bleeding, vasodilated) is treated with fluid resuscitation — IV crystalloid, colloid, or blood products. Excess preload (volume overloaded, pulmonary edema) is treated with diuresis or ultrafiltration. The clinical question is always: will this patient's cardiac output improve with more fluid? The answer is yes (patient is preload responsive) or no (patient is on the flat portion of the Starling curve — more fluid adds pulmonary edema without improving output).
Definition: Afterload is the resistance against which the ventricle must eject — the pressure the ventricle must overcome to open the aortic (or pulmonic) valve and eject blood. Systemic vascular resistance (SVR) is the primary determinant of left ventricular afterload. Pulmonary vascular resistance (PVR) is the primary determinant of right ventricular afterload.
Normal SVR: 800–1,200 dyn·s/cm5. SVR is calculated from: SVR = (MAP − CVP) / CO × 80.
High afterload: Increases the work of the left ventricle. In a patient with impaired contractility (systolic heart failure, post-MI), high afterload reduces stroke volume significantly — the weakened ventricle cannot overcome high resistance. Treatment: afterload reduction with vasodilators (nitroprusside, hydralazine, ACE inhibitors).
Low afterload (vasodilation): Reduces the resistance the ventricle faces. In septic shock, massive vasodilation drops SVR — the heart is actually ejecting well (hyperdynamic), but the vascular tree is too dilated to maintain MAP. Treatment: vasoconstrictors (norepinephrine, vasopressin).
Definition: Contractility (also called inotropy) is the intrinsic ability of the myocardium to generate force at a given preload and afterload. It reflects the calcium cycling and cross-bridge formation within the cardiac myocyte. Contractility is separate from preload — a highly contractile heart ejects more at any given filling pressure than a weakly contractile heart.
Reduced contractility: Cardiogenic shock, systolic heart failure (EF reduced), myocarditis, severe sepsis (myocardial depression), post-ischemia. Treated with inotropes.
| Drug | Mechanism | Primary Effect | Clinical Use |
|---|---|---|---|
| Dobutamine | Beta-1 agonist (primarily); some Beta-2 | Increases contractility + HR; mild vasodilation (Beta-2); decreases afterload slightly | Cardiogenic shock with low CO and elevated SVR; acute decompensated heart failure; dobutamine stress testing |
| Milrinone | Phosphodiesterase III inhibitor | Increases contractility + promotes vasodilation (afterload reduction); "inodilator" | Acute decompensated heart failure; post-cardiac surgery low output syndrome; preferred when tachycardia is a concern (less chronotropy than dobutamine) |
| Dopamine | Dose-dependent: low dose = dopaminergic; moderate = Beta-1; high = Alpha-1 | Low dose: vasodilation of renal/mesenteric. Moderate dose: increased CO. High dose: vasoconstriction + inotropy | Largely replaced by norepinephrine for vasopressor support; still used in some bradycardia management; associated with more arrhythmias than norepinephrine in septic shock |
| Epinephrine | Alpha-1 + Beta-1 + Beta-2 agonist | Potent vasoconstriction + powerful inotropy + chronotropy; increases SVR and CO simultaneously | Anaphylaxis (first-line); cardiac arrest (ACLS); refractory cardiogenic shock; post-ROSC hemodynamic support |
| Norepinephrine | Alpha-1 dominant + Beta-1 | Potent vasoconstriction (increases SVR/afterload); modest inotropy; little chronotropy | First-line vasopressor for septic shock; distributive shock states; preferred over dopamine due to lower arrhythmia risk |
| Vasopressin | V1 receptor on vascular smooth muscle | Pure vasoconstriction independent of adrenergic pathway; no direct inotropic effect | Adjunct vasopressor in septic shock (added to norepinephrine to spare doses); vasodilatory shock states; post-cardiac surgery vasoplegia |
| Phenylephrine | Alpha-1 agonist only | Pure vasoconstriction; no inotropy; reflex bradycardia possible | Vasodilatory hypotension in OR/anesthesia; distributive shock when tachycardia is a problem; spinal anesthesia hypotension |
Heart rate directly affects cardiac output — CO = HR × SV. Within normal ranges, increased heart rate increases CO. However, at very high heart rates, diastolic filling time is reduced, SV drops (the ventricle doesn't fill adequately before the next contraction), and CO may actually fall despite the rate increase. This is why atrial fibrillation with RVR (rapid ventricular response) compromises CO — the high rate without adequate filling reduces SV.
Conversely, severe bradycardia reduces CO by reducing the rate component even with normal SV. Heart block, complete AV dissociation, sinus bradycardia from beta-blocker toxicity, or hypothermia-induced bradycardia all require intervention if CO falls to compromising levels.
In a fully invasively monitored ICU patient (arterial line, PA catheter or PICCO), the hemodynamic profile tells you: Which component of CO is failing? Low MAP with high CO and low SVR = distributive (septic, anaphylactic) → needs vasoconstrictors. Low CO with high SVR and high PCWP = cardiogenic → needs inotropes ± afterload reduction. Low CO with low SVR and low PCWP = mixed hypovolemic + distributive → needs fluids first, then reassess. Low CO with low SVR and low PCWP in the context of obstructive findings = obstructive shock (PE, tamponade, tension pneumothorax) → the vasopressors and fluids are temporizing — the obstruction must be relieved.
Related guides: Acid-base balance | Chest tube care | 12-lead EKG interpretation | CRNA school requirements
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