Cardiovascular Physiology and Hemodynamics

Vocabulary practice flashcards covering cardiac output, stroke volume, Frank-Starling mechanics, Poiseuille's law, and hemodynamics based on the lecture notes.

Cardiac Output ($CO$)

The total volume of blood pumped by the heart each minute, calculated as heart rate multiplied by stroke volume ($CO = HR \times SV$; for example, $75\,\text{beats/min} \times 70\,\text{ml/beat} = 5250\,\text{ml/min}$).

Stroke Volume ($SV$)

The volume of blood ejected by a ventricle with each heart beat; it increases to pump out more blood to prevent heart overfilling and is regulated by end-diastolic volume ($EDV$), total peripheral resistance ($TPR$), and contractility.

Mean Arterial Pressure ($MAP$)

The average pressure in the arterial system across the cardiac cycle, calculated by the formula $MAP = DP + \frac{1}{3}(SP - DP)$; for a blood pressure of $120/80\,\text{mmHg}$, $MAP = 80 + \frac{1}{3}(120 - 80) = 93.33\,\text{mmHg}$.

Preload

Another clinical and physiological term for end-diastolic volume ($EDV$), representing the degree of myocardial stretch prior to contraction.

Total Peripheral Resistance ($TPR$) / Afterload

The resistance or opposition to blood flow throughout the systemic circulation that the heart must overcome in order to pump blood forward.

End-Diastolic Volume ($EDV$)

The total volume of blood in the ventricles at the end of resting diastole immediately before contraction begins, which directly governs resting sarcomere stretch and stroke volume.

Frank-Starling Law of the Heart

The intrinsic myocardial property stating that the force of ventricular contraction varies directly with end-diastolic volume ($EDV$); as ventricular filling increases, cardiac muscle fibers stretch and contract with greater force, resulting in increased stroke volume.

Positive Inotropic Effect

An increase in myocardial contractility and contraction strength induced by norepinephrine and epinephrine, mediated by an increased release and buildup of $Ca^{2+}$ in the sarcoplasmic reticulum ($SR$).

Sodium-Calcium Exchanger ($NCX$) Regulation by Epinephrine

The cellular mechanism in cardiomyocytes where epinephrine closes the sodium-calcium exchanger ($NCX$), leading to an intracellular buildup of $Ca^{2+}$ and a subsequent increase in contractility.

Poiseuille's Law of Flow Rate ($Q$)

The hemodynamic equation $Q = \frac{\Delta P \cdot r^4 \cdot \pi}{\eta \cdot L \cdot 8}$, showing that volumetric fluid flow is directly proportional to the pressure gradient ($\Delta P$) and the fourth power of the vessel radius ($r^4$), and inversely proportional to fluid viscosity ($\eta$) and vessel length ($L$).

Effect of Heart Rate on Ventricular Filling

An extremely rapid heart rate shortens filling time, decreasing venous return, $EDV$, and stroke volume; conversely, a slow heart rate lengthens diastolic filling time, increasing $EDV$ and stroke volume.

Determinants of Venous Return

The physiological factors regulating the rate of blood flow returning to the heart, comprising blood volume (governed by urine and tissue-fluid volumes), breathing (generating negative intrathoracic pressure), and venous pressure (enhanced by sympathetic venoconstriction and the skeletal muscle pump).

Sarcomere Length-Tension Relationship in Myocardium

Before filling at $1.5\,\mu\text{m}$, actin filaments overlap excessively and produce weak contraction force; stretching the sarcomere toward optimal resting lengths ($2.0\,\mu\text{m}$ to $2.4\,\mu\text{m}$) optimizes actin-myosin overlap and maximizes contractile tension.

Gravitational Effect on Dependent Venous Pressure

In an upright standing individual, venous pressure at the feet reaches $100\,\text{mmHg}$, consisting of $90\,\text{mmHg}$ produced by the hydrostatic weight of a $1.5\,\text{m}$ vertical column of blood and $10\,\text{mmHg}$ generated by cardiac contraction.