Ch18 Vascular Physiology

six types of blood vessel found in the circulatory system

elastic, muscular, arterioles, capillaries, venules, veins

elastic arteries

high flow, high pressure, low resistance (large lumen). High elasticity - propel blood along upper arterial tracts by expanding and passively (elastically) rebounding with each
systolic pulse and diastolic ebb to maintain blood pressure and flow (pressure reservoirs).

muscular arteries

high flow, high pressure, low resistance, lower elasticity and more muscular activity to modify flow and pressure to whole organs/parts of body

arterioles

lower flow, lower pressure/high resistance (and high tuning of resistance) – CV system “spends” pressure to move the blood through resistance. The highest drop in pressure occurs
through the arteriolar region though they are a relatively small region of the CV system. The small lumen and high amount of vasodilation/vasoconstriction possible through smooth muscle action here is the main way that the body controls TPR and therefore makes rapid changes to BP. Sympathetic tone is responsible for maintenance of TPR and BP at the arterioles

capillaries

• low flow, low pressure (but still dropping across bed), high surface area

• function as filters for bulk flow into (filtration) and out of (reabsorption) the interstitial fluid of the
  tissues

• diffusion/transport exchange beds for blood gases and nutrients/wastes/signaling molecules

venules

little veins: transition structure between capillaries and veins – have some functional aspects of both depending on conditions

• involved particularly in capillary reabsorption in
  appropriate tissues.

veins

low pressure, high flow (particularly near heart) but low flow RATE, high compliance (high stretchiness/low elasticity), pressure and pressure gradient are low, but with check valves, and muscle and respiration-based pumping they move blood gently back to heart. Function as a volume reservoir – increased pressure (and smooth muscle action in the veins) during physical activity decreases amount of blood in the veins and increases circulatory flow to deliver gases and nutrients
to metabolically active body parts more quickly.

Continuous capillaries

• strong barrier, pinocytic fluid movement, intercellular clefts in most also allow filtration (though tight junctions in brain as part of BBB do not)

• This is the most common, general capillary type

Fenestrated capillaries

• porous barrier with intact basement membrane/glycocalyx filter

• stops most protein but has high bulk fluid movement through fenestrations and clefts, found in areas of high
  filtration and/or reabsorption (kidney, digestive tract, endocrine glands

Sinusoid

very porous, allows unrestricted fluid flow through sinusoids including proteins and even cells, found in bone marrow, liver, spleen, adrenal medulla

venous valves

• Major veins, particularly in the lower body, have “check valves” much like the semilunar valves of the heart in structure

• They prevent backflow in the venous system and facilitate low-pressure fluid movement in the face of body movements and gravitational force.

percentage of volume in arteries vs veins? vessels vs heart? the systemic vs the pulmonary circuit?

75% in systemic, 12% in the pulmonary circuit, 5% in capillaries = actively perfusing tissue and 8% in the heart

60% in systemic venules alone (high compliance vessels, blood reservoir at rest)

resting CO for a typical individual with a heart rate of 70bpm and stroke volume of 75mL

75 mL/beat * 70 beats/min = 5250 mL/min or 5.25 L/min roughly comparable to the entire blood volume of the body ~5L

does the systemic or pulmonary circuit have a larger cardiac output (CO, volume of blood pumped per minute) or is it the same

the output of the two circuits is the same despite the larger volume of blood in the systemic circuit. stroke volume of each ventricle is the same and beating is coordinated.

preload

pressure on the resting heart from the venous return leading to degree of stretch of the heart muscle

frank-starling relationship and what skeletal muscle phenomenon does this resemble

increased preload increases strength of contraction to compensate. (similar to length-tension relationship of skeletal muscle)

resting cardiac muscle SHORTER than optimal, so upon increased stretch contracts much harder (also the range of functional stretch is greater).

afterload

the amount of diastolic pressure exerted on the heart by the arteries essentially the backpressure working against ventricular contraction due to the actions/state of the blood vessels

• aka resistance

high afterload

• increased by high BP, arteriosclerosis, and atherosclerosis/stenosis

• can cause myocardial and cardiac valve damage, heart dysfunction, and even heart failure if untreated

• why doctors are concerned with elevated diastolic pressure

What two volumetric parameters must be subtracted to determine stroke volume (SV)

SV = EDV - ESV

EDV

End-diastolic volume

• highest volume of the ventricle during the cardiac cycle prior to contraction / determined by the extend of venous return (preload)

• mostly controlled by physical activity and SyANS activity

ESV

End-systolic volume

• lowest volume of the ventricle during the cycle at the end of contracting

• how hard the ventricle is working (contractility) and how heard the body is pushing back on the heart

• contractility is altered by SyANS as well as endocrine, and humoral markers

percentage of systemic arterial flow

20 to muscles at rest

25 to abdominopelvic organs (except kidneys)

13 to brain

20 to kidneys

Relationship between pressure, flow, and resistance

Flow = difference in pressure/resistance =
change of MAP/TPR (conceptually)

• Fluid pressure results as flow pushes against resistance

• highest resistance vessels are the arterioles where the blood experiences the largest drop in pressure

• HR and SV changes are mostly about maintaining MAP/ providing adequate flow upon demand

What are short term and long term ways of changing MAP

• TPR controlled by smooth muscle constriction = short term

• Kidney has long term mechanisms

How is MAP calculated

MAP = diastolic pressure + 1/3 pulse pressure (1/3 difference between systolic and diastolic pressure)

Systolic pressure

Pressure at peak of ventricular contraction (related to CO)

Diastolic pressure

pressure when ventricles are relaxed and filling (determined largely by TPR)

Pulse pressure

difference between diastolic and systolic (related to contractility/SV)

Vasomotor tone

• constant level of stimulation of the smooth muscle of the blood vessels by the SyAns through maintenance norepi neurotransmission and maintenance of epinephrine

• blood vessels are a bit constricted at rest

• contributes to BP dropping and also why high BP is a sign of stress

Baroreceptor reflexes

located in the carotid sinus and aortic arch. measure BP and report it to the medullary cardiovascular centers (increased pressure = increased AP frequency) triggers short term effects

• increased pressure increases baroreceptor action potential which increases efferent signals from CV stimulatory center through SyANS

why are baroreceptors ill-suited to correcting chronic hypertension?

CV centers quickly adjust to “new normal” / baroreceptors are only effective at countering changes no unhealthy resting levels of BP (tolerance is responsible for this)

Chemoreceptors

present in the carotid sinus and aortic arch, but also int he brain stem

• measure pH and O2 levels, also measure osmolarity in the brain

• when blood gas concentration changes these will increase the activity of the cardioaccelerator center

• mainly utilized for breathing regulation and respiratory gas exchange

short term endocrine controls of blood pressure

epinephrine, angiotensin II/III, vasopressin (ADH)

Epinephrine

primary hormone of the SyANS / accelerates HR, increases SV and increases vasoconstriction (TPR) all of which increase BP

Angiotensin II/III

part of the RAAS (stimulated by renin) / stimulates aldosterone and also causes vasoconstriction when blood volume/pressure is low

ANGIII = full aldosterone stimulating activity but little vasocostrictive

ANGII = stimulates posterior pituitary to produce ADH and stimulates thirst in the hypothalmus

Vasopressin/ADH

ADH is produced by the posterior pituitary under conditions of low blood pressure/ high osmotic strength

• stimulated additional reabsorption of water directly back into the bloodstream at the kidney

• does NOT rely on moving salt and is the only way the body can correct osmotic problems other than altering thirst

long term endocrine controls of blood pressure

aldosterone, atrial natriuretic peptide, vasopressin/ADH, EPO

Aldosterone

• primary hormone of water/mineral balance in the body + a mineralocorticoid

• increases water retention in the kidneys through reabsorption of sodium

• also increases K+ excretion by the kidney

Atrial natriuretic peptide

ANP is produced by heart, stimulated by increased myocardial stretch in the atrium

• antagonizes aldosterone by decreasing Na+ and H2O reabsorption

Vasopressin

increases water retention in a salt-independent manner. Part of the mechanism for this increases urea retention/trapping in the kidney

EPO

Erythropoietin is a hormone produced by the kidney in response to low partial pressure of O2. EPO increases RBC synthesis in the bone marrow, increasing hematocrit (% of
RBC in the blood) and therefore increasing oxygen transport capacity (VO2max) and aerobic capability (along with other adjustments such as respiratory changes and increased bis-phosphoglycerate unloading of hemoglobin).

Hypertension

High blood pressure (anything over ~ 130/90)

Risk factors for primary hypertension include genetics, stress levels, diet/obesity/diabetes (these all go hand in hand and are sometimes summarized as “metabolic syndrome”), age, and
smoking. Rarely it is caused by a physical problem/obstruction in the major arteries (secondary hypertension).

Treatments include lifestyle changes (better diet, better fitness), lowpressors (ACEi, ARb, CCb, beta-blockers) which lower vasoconstriction and/or CO, and diuretics such as Lasix which lower blood volume.

Shock

the state of acute and severe hypotension leading to a lack of perfusion (lack of adequate blood flow to tissues

Hypovolemic

low blood volume, often due to hemorrhage (severe bleeding)

Anaphylactic

widespread vasodilation due to histamine cascade (severe allergic reaction in bloodstream

neurogenic

ANS disruption – including psychological or “fear” shock

septic

due to widespread infection, particularly in the bloodstream, due to widespread inflammation (local vasodilation is a major mechanism) and due to DIC (intravascular coagulation, clotting blood in the vessels and preventing blood flow to critical organs

cardiogenic

major heart problems – heart attack or heart failure – cannot sustain BP

autoregulation

intrinsic control of blood flow at the local tissue level. This process responds to local nutrient/waste levels, temporary loss of blood flow, and/or increased skeletal muscle
activity and temperature with paracrine factors that strongly vasodilate local vessels, increasing flow to metabolically active/needy tissue

hyperemia

active skeletal muscle decreases nutrients/O2 and increases wastes/CO2, as well as heating up. All of these effects and also paracrine stretch-mediated effects in the blood
vessels themselves stimulate local vasodilation which dramatically (10X!) increases blood flow to active skeletal muscle during activity DESPITE vasoconstrictive effect of SyANS

How much fluid volume filters into the interstitial space at the capillaries each day? How much is reabsorbed? What happens to the excess?

20 L/day is filtered from plasma into ISF at the arterial side of the systemic capillaries (except/in addition to 200 L a day in glomerular capillaries of the kidneys!). Most of this however is
reabsorbed at the venous side of those same systemic capillaries (except again for renal functions which we will see in chapter 24 – the glomerulus does not reabsorb any of the 200 L!). Only 3 L per day net filtration out of plasma into ISF remains – this becomes lymph, unless swelling/edema are occurring, and is returned to venous circulation eventually through lymphatic drainage into the subclavian vein.

Starling forces

hydrostatic (bulk) and osmotic (chemical/solute) pressures across the capillary beds

• Hydrostatic pressure is ~ 35 mmHg from blood to ISF in arterial side, ~ 17 mmHg on venous
  side

• osmotic pressure remains essentially constant (mostly determined by blood proteins – albumins and globulins that do not cross ordinary capillaries) at ~ 25 mmHg from ISF to blood (opposes hydrostatic flow).

• This is why fluid flows out of plasma to ISF at start of capillaries (net + 10 mmHg outward from
  blood) and then most flows back from ISF into blood at end of capillaries (net -8 mmHg inward
  to blood)