Lecture Notes: Cardiovascular Regulation, Fluid Balance, and Microcirculation

Vocabulary flashcards covering MAP/CO/TPR, neural and hormonal control of BP, capillary exchange, Starling forces, fluid compartments, osmosis, and microcirculation.

Mean arterial pressure (MAP)

Average arterial pressure; MAP = CO × TPR; BP is the regulated variable, controlled by short-term neural and long-term renal mechanisms; not directly HR, SV, or TPR.

Cardiac Output (CO)

Volume of blood pumped per minute; CO = HR × SV.

Total Peripheral Resistance (TPR)

Overall resistance to blood flow in the systemic circulation; mainly controlled by arteriolar tone and affects MAP.

Nucleus tractus solitarius (NTS)

Main brainstem integrator of cardiovascular sensory input (baroreceptors, chemoreceptors).

Vasomotor center

Brainstem region that regulates sympathetic outflow to vessels, thereby modulating TPR.

Cardiac centers

Medullary centers: cardioinhibitory (parasympathetic, decreases HR) and cardio stimulatory (sympathetic, increases HR and SV).

Baroreceptors

High-pressure stretch receptors that detect BP changes and signal NTS to adjust HR, contractility, and vascular tone.

Carotid sinus

Baroreceptor location at the carotid bifurcation (innervated by CN IX).

Aortic arch baroreceptors

Baroreceptors in the aortic arch (innervated by CN X).

Peripheral chemoreceptors

Carotid bodies that sense low PO2, high PCO2, and low pH; influence ventilation and cardiovascular output via NTS.

Low-pressure atrial receptors

Receptors in atria and venous reservoirs that sense venous return; influence ANP, ADH, RAAS, and renal SNA.

Renin–angiotensin–aldosterone system (RAAS)

Hormonal cascade activated by low BP/BV; renin converts angiotensinogen to Ang I, ACE converts to Ang II, raising TPR and promoting Na/H2O retention via aldosterone.

Renin

Kidney enzyme that cleaves angiotensinogen to angiotensin I.

Angiotensinogen

Liver-derived precursor protein; substrate for renin to form angiotensin I.

Angiotensin I

Inactive peptide converted to angiotensin II by ACE.

Angiotensin II

Potent vasoconstrictor; increases TPR, stimulates aldosterone, promotes Na/H2O retention; raises MAP; reduces bradykinin.

Angiotensin-converting enzyme (ACE)

Enzyme converting Angiotensin I to Angiotensin II; also degrades bradykinin.

Aldosterone

Adrenal cortical hormone increasing Na+ and water reabsorption in kidney; expands blood volume.

Bradykinin

Vasodilator peptide; its effects are opposed by Ang II; contributes to vasodilation when present.

Vasopressin (ADH/AVP)

Posterior pituitary hormone; increases water reabsorption via V2 receptors; can cause vasoconstriction via V1 receptors; raises blood volume and MAP.

Atrial natriuretic peptide (ANP)

Hormone from atrial myocytes with atrial stretch; promotes natriuresis and diuresis; reduces blood volume and MAP; counteracts RAAS and vasopressin.

Brain natriuretic peptide (BNP)

Ventricular natriuretic peptide; marker for heart failure; similar natriuretic actions to ANP.

Diuretics

Drugs that promote salt and water excretion to lower BP.

ACE inhibitors

Drugs that block ACE, reducing Ang II formation and lowering BP.

ARBs

Angiotensin II receptor blockers; prevent Ang II action and lower BP.

Renin inhibitors

Drugs that inhibit renin activity to suppress RAAS and lower BP.

BNP testing

Laboratory test used to diagnose or monitor heart failure.

Hypotension

Low blood pressure; defined as systolic BP < 90 mmHg and/or diastolic BP < 60 mmHg; can cause symptoms like dizziness.

Shock

Inadequate tissue perfusion leading to potential cellular injury; may be reversible or irreversible.

Hypovolemic shock

Shock due to significant blood or fluid loss (hemorrhage, dehydration), with reduced BV and MAP.

Distributive shock

Shock with low systemic vascular resistance (sepsis, anaphylaxis); BP drop with relative hypovolemia.

Cardiogenic shock

Shock due to heart pump failure; severely reduced CO.

Compensated hemorrhage

Early stage (<25% blood loss) where baroreflex maintains MAP.

Progressive hemorrhage

Further blood loss (≈30%+); risk of irreversibility without therapy.

Irreversible hemorrhage

Severe blood loss (~30–40%) with poor recovery despite therapy.

Atrial reflex (cardiopulmonary reflex)

Reflex responses increasing vasopressor activity to preserve BP during hemorrhage.

Capillary fluid shift

Movement of fluid between interstitial and intravascular compartments during hemorrhage.

Skeletal muscle pump

Rhythmic muscle contractions squeeze veins to enhance venous return; assisted by valves.

Respiratory pump

Inspiration lowers thoracic pressure and raises abdominal pressure to promote venous return.

Orthostatic hypotension

BP drop on standing due to gravity and venous pooling; dizziness or fainting.

Vasovagal syncope

Fainting triggered by emotional stress; increased vagal tone lowers HR/CO and MAP.

Dynamic exercise response

During exercise CO increases (HR↑, SV↑); muscle blood flow rises; MAP increases modestly due to muscle vasodilation.

Endothelium

Innermost lining of vessels; releases vasodilators (NO, PGI2) and vasoconstrictors (endothelin); regulates exchange.

Elastic tissue

Elastin-containing tissue in arteries; provides compliance and energy storage.

Vascular smooth muscle cells

Circumferential muscle that contracts/relaxes to change vessel diameter.

Fibrous tissue

Collagen-rich layer providing tensile strength and limits stretch.

Resistance vessels

Small arteries/arterioles; main site of vascular resistance; regulate TPR and blood flow distribution.

Compliance

Ability of a vessel to stretch; C = ΔV/ΔP.

Arteries vs veins compliance

Arteries have low compliance; veins have high compliance and can store large blood volumes.

Systolic pressure (SP)

Peak arterial pressure during ventricular systole.

Diastolic pressure (DP)

Lowest arterial pressure during ventricular diastole.

Pulse pressure (PP)

Difference between systolic and diastolic pressure; PP = SP − DP.

Mean arterial pressure approximation

MAP ≈ DP + (1/3) × PP; practical estimation of MAP.

Posture effects on venous pressure

Standing causes gravitational pooling in legs, lowering venous return and affecting MAP.

Venous return enhancement

Mechanisms like skeletal muscle pump and respiratory pump increase venous return to the heart.

Microcirculation

Small vessels (arterioles, capillaries, venules) and neighboring lymphatics; site of exchange.

Capillaries

Smallest vessels with endothelial lining; site of nutrient and gas exchange; slow flow allows diffusion.

Continuous capillaries

Capillaries with tight junctions; found in muscle, skin, CNS (BBB in CNS).

Fenestrated capillaries

Capillaries with pores (fenestrae) to increase permeability; found in kidneys, endocrine glands, intestines.

Discontinuous capillaries (sinusoids)

Wide gaps between endothelial cells; allow large molecules to pass; found in liver, spleen, bone marrow.

Nutritive flow

Capillary flow that supplies nutrients and gases to tissues; regulated by precapillary sphincters.

Non-nutritive flow

Flow path that bypasses capillaries via metarterioles during low metabolic demand.

Capillary permeability variability

Permeability differs by organ; CNS has tight endothelium forming the blood-brain barrier.

Transcapillary movement of solutes

Diffusion (main), plus pinocytosis; diffusion follows Fick's law.

Diffusion (Fick's law)

Movement of solutes down their concentration gradient across a membrane; rate depends on diffusion coefficient, gradient, surface area, and distance.

Pinocytosis

Vesicular transport of large, lipid-insoluble molecules across capillary walls; minor role.

Transcapillary fluid exchange (Starling forces)

Forces governing filtration/absorption: Pc, Pi, πc, πi.

Capillary hydrostatic pressure (Pc)

Pressure within capillaries favoring filtration into the interstitium.

Interstitial hydrostatic pressure (Pi)

Pressure in the interstitium opposing filtration.

Capillary oncotic pressure (πc)

Osmotic pressure exerted by plasma proteins; promotes absorption into capillaries.

Interstitial osmotic pressure (πi)

Oncotic pressure from interstitial proteins; favors filtration.

Net Filtration Pressure (NFP)

NFP = (Pc − Pi) − (πc − πi); positive means filtration, negative means absorption.

Lymphatic system

Parallel system that returns excess interstitial fluid to the circulation; contains valves and one-way flow.

Lymph flow

Propelled by lymphatic pump, skeletal muscle activity, and body movement; interstitial hydrostatic pressure drives flow.

Edema

Abnormal accumulation of interstitial fluid due to excessive filtration or impaired lymph drainage; causes include increased Pc, increased πi, decreased πp, and lymphatic obstruction.

Edema causes: increased Pc

Conditions like hypertension, heart failure, local inflammation raise capillary pressure and filtration.

Edema causes: increased capillary permeability (Kf)

Inflammation or burns increase leakiness and protein exit, reducing absorption.

Edema causes: decreased plasma protein (πp)

Liver, kidney disease, or malnutrition lower plasma protein concentration and capillary reabsorption.

Edema causes: increased interstitial protein (πi)

Interstitial protein accumulation raises interstitial oncotic pressure, promoting edema.

Edema causes: obstruction of lymphatic drainage

Filariasis or lymph node damage prevents fluid/protein return, causing edema.

Effective (non-permeant) osmoles

Solutes that cannot freely cross cell membranes; create lasting osmotic gradients (e.g., Na+, K+, Cl−).

Ineffective (permeant) osmoles

Solutes that freely cross membranes; temporary osmotic gradients that dissipate (e.g., urea, glucose after metabolism).

Total body water (TBW)

Approximately 60% of body weight; ~42 L in a 70 kg person; divided into compartments.

Intracellular Fluid (ICF)

Fluid inside cells; about 2/3 of TBW.

Extracellular Fluid (ECF)

Fluid outside cells; about 1/3 of TBW; subdivided into interstitial fluid and plasma.

Interstitial fluid (IF)

Fluid bathing cells; ~3/4 of ECF.

Plasma

Fluid component of blood; ~1/4 of ECF.

Isotonic saline effect on compartments

Increases ECF volume only; no net change in ICF.

NaCl gain effect on compartments

Increases ECF volume and osmolarity; water shifts from ICF to ECF; ICF volume decreases.

Isotonic permeable solute injection

Solute initially increases ECF osmolarity; as it enters cells, osmolarity equilibrates and TBW increases.

D5W (isotonic glucose) behavior

Glucose acts osmotically initially but is metabolized; ends up drawing water into both ECF and ICF.

Big picture: TBW compartments distribution

ICF is largest (≈2/3 of TBW); ECF ≈ 1/3 of TBW; IF is majority of ECF; plasma is smallest part of ECF.