Hypoalbuminemia is a common complication among hospitalized patients. Albumin is characterized by its non-specific binding to drugs, which makes hypoalbuminemia of concern among clinicians. Significant care should be applied to drugs of high protein binding capacity where hypoalbuminemia tends to cause pharmacokinetic changes and, consequently, pharmacodynamic alterations. These changes require drug dose adjustments based on albumin level and kidney function as well. This case report highlights an explanation of events most likely occurring when acute hypoalbuminemia is recorded among critically ill patients. Ivabradine was a drug of choice to control inappropriate sinus tachycardia in a critically ill cancer patient where acute hypoalbuminemia was detected while kidneys were functioning properly (determined by eGFR) and liver enzymes, including SGOT and SGPT showed normal values. The effect of ivabradine was easily detected by monitoring the heart rate in the intensive care unit. Pharmacokinetic changes associated with acute hypoalbuminemia observed in the case were associated with a decrease in heart rate, which might be due to an increase in tissue concentration of ivabradine as a highly protein-bound drug, which led to an increase in volume of distribution and hence increased activity of the drug as long as liver and kidney functions remained intact. The rapid increment in fraction unbound drug was followed by an escalation of drug elimination where heart rate increased, then returned to normal values. This is how our body maintains homeostasis. Integrating different pharmacokinetic parameters represents an essential step in decision-making about dose adjustment in hypoalbuminemia.