peripheral circulation & respiratory 3

Why must cardiac output be distributed differently at rest vs. during exercise?

Because cardiac output is distributed peripherally according to the metabolic and functional demands of organs and tissues

At rest, what percentage of cardiac output goes to skeletal muscle, and what is total CO?

About 20% of CO; total CO = 30 L/min (6 L/min to skeletal muscle)

During exercise, what percentage of cardiac output goes to skeletal muscle, and what is total CO?

About 71% of CO; total CO = 150 L/min (106 L/min to skeletal muscle, an 18-fold increase)

Why is regulation of arterial pressure needed?

To provide organs with a constant perfusion pressure so each organ system can alter its resistance to achieve desired flow in response to metabolic needs, hemorrhage, and long-term blood volume states — optimizing cardiovascular efficiency and minimizing cardiac, vascular, and renal damage

What are baroreceptors?

Specialized nerve endings sensitive to blood pressure changes that detect stretch of blood vessel walls and relay signals to the CNS

Where are high-pressure baroreceptors located?

In the carotid sinus (at the bifurcation of external and internal carotids) and in the aortic arch

What is another name for high-pressure baroreceptors?

"Pressure receptors"

Which cranial nerve carries carotid sinus baroreceptor signals to the CNS?

The carotid sinus nerve, a branch of the glossopharyngeal nerve (Cranial Nerve IX)

Which cranial nerve carries aortic arch baroreceptor signals to the CNS?

The vagus nerve (Cranial Nerve X), via the aortic nerve

What divisions of the ANS make up the efferent pathway of the baroreceptor reflex?

Both the parasympathetic and sympathetic divisions

What are the peripheral effectors in the neural control of arterial pressure?

The heart, the arteries and veins, and the adrenal medulla

Describe the baroreceptor reflex response when blood pressure falls below normal

Decreased carotid sinus/aortic arch receptor potential → decreased afferent nerve firing → cardiovascular center response: increased sympathetic cardiac and vasoconstrictor activity, decreased parasympathetic activity → increased heart rate, stroke volume, and arteriolar/venous vasoconstriction → increased CO and SVR → increased BP toward normal

What is the equation relating blood pressure to cardiac output and resistance?

BP = CO × SVR (systemic vascular resistance)

Where are low-pressure baroreceptors located?

Within the great veins, the atria, and the pulmonary vasculature — largely on the low-pressure venous side of the systemic circulation

What is another name for low-pressure baroreceptors?

"Volume receptors"

What effects do low-pressure baroreceptors have?

Both circulatory and renal effects — they change hormone secretion controlling salt/water retention and intake, allowing long-term regulation of blood volume and mean blood pressure

How much change in venous volume is generally required to activate low-pressure baroreceptors?

A change of 5–10%

What are the two hormones central to long-term regulation of arterial blood pressure discussed in this lecture?

Angiotensin II and Aldosterone

What triggers renin release from the kidney?

A fall in arterial blood pressure below normal

What does renin act on, and what is produced?

Renin acts on angiotensinogen (renin substrate, produced by the liver) to produce Angiotensin I

What converts Angiotensin I to Angiotensin II, and where does this occur?

Angiotensin Converting Enzyme (ACE), primarily in the lung

What are the main effects of Angiotensin II?

Vasoconstriction (increasing SVR) and stimulation of aldosterone release from the adrenal cortex

What does aldosterone do?

Increases renal Na+ and water reabsorption, increasing blood volume

How does the renin-angiotensin-aldosterone system ultimately raise blood pressure?

Increased blood volume → increased cardiac output; plus Angiotensin II-induced vasoconstriction → increased SVR; together (MABP = CO × SVR) restore blood pressure toward normal

What is Atrial Natriuretic Peptide (ANP) and what stimulates its release?

A hormone released from the heart in response to atrial distension, sympathetic stimulation, Angiotensin II, and endothelin

What type of vasodilator is ANP?

A direct vasodilator

What effect does ANP have on urinary sodium and water excretion?

It increases urinary sodium and water excretion (natriuresis and diuresis)

How does ANP affect Angiotensin II production?

It indirectly suppresses Angiotensin II production

What are the net cardiovascular/renal effects of ANP?

To lower blood volume and reduce systemic blood pressure via decreased SVR, decreased CVP, decreased CO, increased GFR, decreased renin release, and decreased aldosterone/Angiotensin II

What enzyme degrades ANP?

Neprilysin (NEP), a peptidase

What is vascular (basal) tone?

A normal state of partial constriction of arteriolar smooth muscle that establishes a baseline of arteriolar resistance

What two factors are responsible for basal vascular tone?

Arteriolar smooth muscle myogenic activity (arising in the muscle itself) and tonic sympathetic ANS activity

What receptor mediates vasoconstriction from basal tone, and what is its effect?

Alpha1 receptor activity, which increases resistance and decreases blood flow through the vessel

What receptor mediates active vasodilation, and what is its effect?

Beta2 receptor activity (and cholinergic receptor activity), which decreases resistance and increases blood flow

What is passive vasodilation?

A decrease in alpha1 receptor activity combined with passive distension from blood pressure, leading to decreased resistance and increased blood flow

Describe the three-tiered hierarchy of vascular control

Top tier (extrinsic): vasomotor nerves and hormones (e.g., epinephrine, norepinephrine, angiotensin II) under brain control; Middle tier (intrinsic): local factors produced within the tissue; Bottom tier (intrinsic): myogenic response

What is the top tier of vascular control and what brings it under central control?

Extrinsic regulation by vasomotor nerves and hormones (epinephrine, norepinephrine, angiotensin II), bringing vascular regulation under control of the brain

What are the chief vasodilators of endothelial origin in the middle (local factor) tier of vascular control?

Nitric oxide (NO), EDHF, prostacyclin, and endothelin

What are examples of functional hyperemia factors in the middle tier of vascular control?

CO2, lactate, adenosine, and K+

What are examples of autacoids involved in local vascular control?

Histamine, bradykinin, serotonin, thromboxane, and Platelet Activating Factor

What is the Bayliss myogenic response?

Vasoconstriction of resistance vessels in response to increased perfusion pressure and vessel stretch, limiting the distension-associated increase in blood flow

What is autoregulation?

The intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure

What happens to arterial PO2 and PCO2 during hyperventilation?

PO2 increases (excessive O2 uptake) and PCO2 decreases (excessive CO2 removal)

What happens to arterial PO2 and PCO2 during hypoventilation?

PO2 decreases and PCO2 increases

What is the primary stimulus for hypoxic pulmonary vasoconstriction?

Low airway (alveolar) PO2

Describe the mechanism and purpose of hypoxia-induced pulmonary vasoconstriction

As ventilation decreases to an alveolus, its PO2 falls, increasing vascular resistance in vessels perfusing that alveolus and redirecting blood flow to better-ventilated regions — maximizing gas exchange by matching ventilation and perfusion

What does the Ventilation (V) / Perfusion (Q) ratio determine?

The efficiency of gas exchange in the lungs

Why do upper portions of the lung tend to be over-ventilated relative to perfusion?

Blood flow favored by gravity concentrates perfusion in lower lung regions, leaving upper regions relatively over-ventilated

Why do lower portions of the lung tend to be over-perfused?

Because blood flow is favored by gravity in the lower lung regions

What is an "absolute shunt" in V/Q mismatching?

No ventilation to an alveolus (A) but uniform blood flow to both A and B — a waste of perfusion

What is "alveolar dead space" in V/Q mismatching?

No blood flow to an alveolus (A) but uniform ventilation to both A and B — a waste of ventilation

What two types of receptors provide feedback for respiratory control?

Mechanoreceptors in the lung and chest wall (responsive to lung expansion) and chemoreceptors in the peripheral circulation (responsive to O2, CO2, and blood pH changes)

Where do respiratory mechanoreceptor and chemoreceptor signals communicate to?

The medullary respiratory center in the brainstem

What is the Hering-Breuer reflex also known as?

The inspiratory-inhibitory reflex or inflation reflex

What receptors mediate the Hering-Breuer reflex and where are they located?

Pulmonary stretch (mechano-) receptors located in the small airways, stimulated by lung inflation

What nerve carries the afferent limb of the Hering-Breuer reflex?

The afferent vagus nerve

What is the function of the Hering-Breuer reflex?

It inhibits inspiratory activity in response to lung distention, protecting the lungs from over-inflation and contributing to regularity of respiratory rhythm

What happens to arterial PCO2 during hypoventilation and how does the body respond?

Arterial PCO2 rises, increasing arterial H+ concentration and CO2/H+ in cerebrospinal fluid, stimulating peripheral chemoreceptors (carotid bodies) and central chemoreceptors, which stimulate medullary inspiratory neurons and increase ventilation

How does increased ventilation provide negative feedback in the hypoventilation reflex response?

Increased ventilation decreases PCO2, providing negative feedback to reduce the stimulus

What are the four types of hypoxia?

Arterial hypoxia/hypoxemia, anemic hypoxia, ischemic hypoxia, and histotoxic hypoxia

What defines arterial hypoxia/hypoxemia and what causes it?

Inadequate oxygenation of arterial blood, due to inspiratory or alveolar defects that reduce arterial PO2 and decrease percentage saturation of hemoglobin

What defines anemic hypoxia and what are two causes?

Insufficient amount of functional hemoglobin; caused by decreased Hb concentration (reducing O2 carrying capacity) or carbon monoxide poisoning (which occupies Hb's O2 binding sites)

What defines ischemic hypoxia and give an example cause?

Inadequate tissue perfusion; e.g., decreased cardiac output reducing blood flow

What defines histotoxic hypoxia and give an example cause?

Inactivation of certain metabolic enzymes (e.g., those involved in mitochondrial respiration); e.g., cyanide poisoning, where O2 supply is adequate but tissue utilization of O2 is decreased