Blood Pressure Regulation, Hypertension, and Shock

Vocabulary flashcards covering key terms from the lecture notes.

Compliance

The ability of a blood vessel wall to expand and contract with changes in pressure; high pressure/volume tends to decrease compliance.

Distensibility

The ease with which a vessel wall stretches in response to pressure; veins are more distensible than arteries (about 8x).

Arterial distensibility

The ability of arteries to distend to accommodate the pulsatile output of the heart.

Venous distensibility

The ability of veins to distend to store blood; veins serve as a reservoir.

Compliance vs. distensibility

Compliance is the overall change in volume with pressure; distensibility is the fractional change in volume per unit pressure.

Transmural pressure

The pressure difference across the vessel wall (inside pressure minus outside pressure).

Driving pressure

The pressure gradient that drives blood flow, typically the difference between arterial and venous pressures.

Recumbent vs upright (orthostasis)

Gravity creates hydrostatic pressure differences when upright; recumbent minimizes these differences.

Orthostatic challenge

Physiological demand when standing that redistributes blood and challenges venous return and cardiac output.

Dichrotic notch

Notch on the arterial pressure waveform signaling aortic valve closure.

Pulse pressure

SBP minus DBP; determined by stroke volume, arterial compliance, and the character of left-ventricular ejection.

Arterial compliance

The ability of the arterial wall to expand with pressure changes to smooth flow.

Arterial stiffness

Increased arterial tone or disease reducing arterial compliance, often increasing pulse pressure.

Arterial vs. venous flow (wave transmission)

Pressure waves travel ahead of actual blood flow; damping occurs in small vessels but overall compliance can increase due to parallel pathways.

Baroreceptors

Pressure-sensitive receptors (carotid sinus, aorta) that regulate blood pressure via autonomic reflexes.

Autonomic reflexes

Reflexes (baroreceptor, CNS responses) that adjust heart rate, vascular tone, and stroke volume to maintain MAP.

Renin-angiotensin system

Kidney-derived renin leads to angiotensin II formation, causing vasoconstriction and Na+/H2O retention, raising BP.

Angiotensin II

Potent vasoconstrictor in the renin-angiotensin system; promotes aldosterone release and water retention.

Volume loading hypertension

Long-term hypertension driven by increased extracellular fluid volume from reduced renal mass and high salt intake.

One kidney Goldblatt hypertension

Experimental model: renal artery constriction causes renin-angiotensin–mediated hypertension with subsequent fluid retention.

White coat hypertension

Elevated clinic BP with normal home BP; ~20% of mild hypertension cases; home monitoring recommended.

Ambulatory blood pressure monitoring (ABPM)

24-hour BP monitoring to assess true daily BP patterns, including nocturnal dipping.

Nocturnal dipping

Normal drop in BP during sleep; non-dippers or inverted dippers indicate altered BP regulation.

Pulse pressure determinants

Determined by stroke volume, arterial compliance, and the nature of the ejection; influences arterial pressure waveform.

Mean arterial pressure (MAP)

A weighted average pressure in the arteries during a single cardiac cycle; diastolic pressure correlates well with MAP in aging.

Essential hypertension

Hypertension with no identifiable cause (~95%); heredity and environment implicated; renin often normal.

Secondary hypertension

Hypertension due to identifiable causes (renal disease/stenosis, catecholamine-secreting tumors, coarctation, primary aldosteronism).

Shock

Peripheral circulatory failure with inadequate tissue perfusion, leading to hypoxia and organ dysfunction.

Hypovolaemic shock

Shock from reduced circulating blood volume (e.g., hemorrhage); >10% CO falls; 35–45% blood loss can collapse MAP.

Cardiogenic shock

Shock from impaired cardiac pump function (infarction, valve dysfunction, arrhythmias).

Distributive shock

Shock due to maldistribution of blood flow: septic, anaphylactic, or neurogenic causes.

Stages of shock

Non-progressive (compensation), Progressive (deterioration), Irreversible (death despite intervention).

Reflex compensation in shock

Baroreceptor/CNS reflexes, Angiotensin, Vasopressin responses to low MAP to maintain perfusion.

Renal function curve

Relationship showing how urine output increases with MAP; rightward shift with reduced renal mass.

Volume loading hypertension vs autoregulation

Initial driver is increased extracellular fluid and CO; baroreceptors reset; long-term BP elevation via increased TPR due to autoregulation.