hemodynamics phys

Pulse Pressure (PP) Equation

Pulse Pressure = Systolic Pressure - Diastolic Pressure (mm Hg) (e.g., 120 - 90 = 30 mm Hg).

Mean Arterial Pressure (MAP) Equation & Calculation

MAP = Diastolic Pressure + [1/3 x (Systolic Pressure - Diastolic Pressure)]. Example for 120/90: 90 + [1/3 x 30] = 100 mm Hg.

Why MAP Weights Diastolic Pressure Heavily

Diastole takes up roughly 2/3 of the cardiac cycle, while systole takes up roughly 1/3, so average perfusion pressure over time is closer to diastolic pressure.

Compliance vs Elasticity in Large Arteries

Compliance (distensibility during systole) limits systolic pressure spikes (~120 mm Hg). Elasticity (recoil during diastole) sustains driving pressure (~80 mm Hg) to maintain continuous blood flow.

Effect of Atherosclerosis on Blood Pressure

Atherosclerosis hardens arteries, decreasing compliance and elasticity. Decreased compliance causes systolic blood pressure to rise significantly.

Poiseuille's Law & Vascular Resistance

Resistance R ∝ (Length x Viscosity) / Radius^4. Vessel radius has the biggest effect on resistance because it is raised to the 4th power (halving radius increases resistance 16-fold).

Vasoconstriction vs Vasodilation Effects

Vasoconstriction decreases vessel radius -> increases resistance -> increases blood pressure. Vasodilation increases vessel radius -> decreases resistance -> decreases blood pressure.

Blood Velocity vs Total Cross-Sectional Area

Blood flow velocity is LOWEST in capillaries because capillaries have the HIGHEST total cross-sectional area, allowing adequate time for gas and nutrient exchange.

Capillary Wall Structure

Consists solely of a single endothelial cell layer and basement membrane; contains NO smooth muscle.

Starling Forces: Hydrostatic vs Colloid Osmotic Pressures

Hydrostatic Pressure (HP) is a PUSHING force exerted by fluid against vessel walls. Colloid Osmotic Pressure (COP) is a PULLING force exerted by non-permeable plasma proteins (albumin).

Capillary Hydrostatic Pressure (HPb) Trend

HPb is HIGHER at the arterial end (~35 mm Hg) and DROPS significantly at the venous end (~16 mm Hg) as fluid leaves.

Capillary Blood Colloid Osmotic Pressure (COPb) Trend

COPb remains EQUAL and relatively high (~26 mm Hg) across both arterial and venous ends because plasma proteins do not cross capillary walls.

Net Filtration Pressure (NFP) Equation

NFP = (Pressures Filtering Out) - (Pressures Reabsorbing In) = (HPb + COPif) - (COPb + HPif).

Net Filtration Pressure at Arterial End

NFP = (35 + 5) - (26 + 0) = +14 mm Hg (Positive NFP = Net Filtration of fluid OUT into tissue).

Net Filtration Pressure at Venous End

NFP = (16 + 5) - (26 + 0) = -5 mm Hg (Negative NFP = Net Reabsorption of fluid BACK into capillary).

Factors Increasing Venous Return & Stroke Volume

Increased total blood volume, skeletal muscle pump, respiratory pump, and venoconstriction increase venous return -> increases EDV -> increases stretch -> increases SV (Frank-Starling Law). Homeostatically Regulated Cardiovascular Variables

Baroreceptor Reflex Response to High Blood Pressure

High BP increases baroreceptor firing in carotid sinus/aortic arch -> cardiovascular center increases parasympathetic output (ACh to SA node) and decreases sympathetic output -> lowers HR, CO, and BP. Baroreceptor Reflex Response to Low Blood Pressure

Endocrine Regulation: ADH (Vasopressin) Mechanism

Hypothalamic osmoreceptors detect increased blood osmolarity or low BP -> posterior pituitary secretes ADH -> ADH inserts aquaporins in kidney collecting ducts -> increases water reabsorption -> normalizes volume.

Endocrine Regulation: RAAS Cascade

Kidney JGA detects low blood volume/pressure -> releases Renin -> generates Angiotensin II (vasoconstriction) -> stimulates Aldosterone release from adrenal cortex -> increases Na+ and H2O reabsorption in distal tubules.

Physiological Rationale for Salt Reduction & Diuretics in Hypertension

High salt increases water retention, raising blood volume and pressure. Decreasing salt intake reduces water retention; diuretics promote renal fluid excretion, both decreasing blood volume and pressure.