Module 9 Study Guide - Physiology I

Everything above, compressed to what you should be able to reproduce without the slides in front of you.

Core ideas¶

Autonomic pathways are two neurons in sequence. Parasympathetic is long-short with ACh at both synapses. Sympathetic is short-long with ACh at the ganglion and norepinephrine at the target. The adrenal medulla route turns the sympathetic signal into circulating hormones.
The SA and AV nodes have balanced dual innervation. The myocardium, arteries, and veins are mostly sympathetic.
Sympathetic stimulation raises blood pressure five ways: heart rate, lusitropy, venoconstriction and venous return, contractility, and arterial vasoconstriction. Parasympathetic stimulation lowers it only through heart rate, plus the withdrawal of sympathetic effects.
Baroreceptors and cardiopulmonary receptors both sense stretch. In high-pressure arteries stretch stands in for pressure. In low-pressure atria, vena cavae, and pulmonary vessels stretch stands in for volume.
The baroreflex runs from the carotid sinus (CN IX) and aortic arch (CN X) to the solitary nucleus and tract, then splits: nucleus ambiguus drives parasympathetic outflow, and the CVLM inhibits the sympathetic driver, the RVLM.
A fall in pressure silences the baroreceptors, which disinhibits the RVLM and removes parasympathetic outflow. The fall-in-pressure response matters more because brain perfusion is at stake.
Without a baroreflex, a 500 mL class one hemorrhage drops MAP from 100 to 65 mmHg. With it, MAP holds at 99 mmHg.
The Bainbridge reflex raises heart rate when atrial filling rises, matching outflow to inflow. Respiratory sinus arrhythmia is the Bainbridge reflex following breathing.
The same rise in venous return drives the baroreflex to lower heart rate and the Bainbridge reflex to raise it. The baroreflex dominates when volume is low, the Bainbridge reflex when volume is high.
Neural reflexes are instant, short-lived band-aids. Endocrine reflexes are delayed and long-term, and often fix the root cause.
Vasopressin and the renin-angiotensin system fix low BP and BV. ANP fixes high BP and BV and is the mirror image of vasopressin and aldosterone.
Venous return drives right atrial pressure, which drives cardiac output. Preload is the coupling factor, and the two flows must match at steady state.
Cardiac curve shifts up or down with contractility, heart rate, and afterload. Venous return curve shifts in parallel with volume or compliance and changes slope with resistance.
The intersection of the cardiac and venous return curves is the steady-state operating point.

Key terms¶

Preganglionic / postganglionic neuron: First neuron, spinal cord to ganglion / second neuron, ganglion to target tissue.
Cholinergic: Related to acetylcholine. Nicotinic at autonomic ganglia, muscarinic at parasympathetic targets.
Adrenergic receptors: Alpha-1, alpha-2, beta-1, beta-2. Norepinephrine prefers alpha-1, alpha-2, beta-1. Epinephrine prefers alpha-1, beta-1, beta-2.
Adrenal medulla: Central region of the adrenal gland. Releases about 80% epinephrine and 20% norepinephrine into the blood.
Chronotropy: Effect on heart rate, at the SA node.
Dromotropy: Effect on conduction velocity through the AV node.
Inotropy / lusitropy: Force of contraction / completeness and speed of relaxation.
Venoconstriction: Sympathetic contraction of venous smooth muscle. Lowers venous volume and compliance, raises venous pressure and venous return.
Baroreflex: Negative feedback reflex that defends arterial pressure.
High-pressure baroreceptors: Stretch receptors in the carotid sinus and aortic arch.
Carotid sinus: Slight swelling at the base of the internal carotid. Innervated by a glossopharyngeal branch.
Solitary nucleus and tract: Medullary region that receives baroreceptor input and stimulates the CVLM and nucleus ambiguus.
Nucleus ambiguus: Drives parasympathetic outflow to the SA node.
CVLM / RVLM: Caudal ventrolateral medulla, inhibits the RVLM / rostral ventrolateral medulla, drives sympathetic outflow to all cardiovascular tissues.
Disinhibited: Freed from inhibition. The RVLM when baroreceptor firing stops.
Atrial stretch reflex: Umbrella term for neural and endocrine loops that defend blood volume.
Cardiopulmonary (low-pressure) baroreceptors: Stretch receptors in the atria, vena cava junction, pulmonary vessels, and right ventricle. Stretch here means volume.
Bainbridge reflex: Neural subset of the atrial stretch reflex. More atrial filling raises heart rate.
Respiratory sinus arrhythmia: Heart rate rising with each breath in and falling with each breath out.
Arginine vasopressin (ADH): Posterior pituitary hormone. Powerful vasoconstriction and renal water retention.
Renin: Kidney enzyme that converts angiotensinogen to angiotensin I.
ACE: Angiotensin converting enzyme, concentrated in pulmonary vessels. Converts angiotensin I to angiotensin II.
Angiotensin II: Hormone that drives thirst, AT₁ vasoconstriction, sympathetic activity, and vasopressin and aldosterone release.
Aldosterone: Hormone that retains Na⁺ at the kidney. Water follows.
Atrial natriuretic peptide (ANP): Released by atrial myocytes on stretch. Vasodilation, natriuresis, renin suppression.
Natriuresis: Urinary loss of sodium ions.
Cardiac function curve: Cardiac output against right atrial pressure.
Venous return (vascular function) curve: Venous return against right atrial pressure, after flipping the axes.
Mean systemic filling pressure: The equal pressure everywhere in a no-flow circulation. The x-intercept of the venous return curve.
Operating point: Where the cardiac and venous return curves intersect.

Numbers worth knowing¶

Adrenal hormone, epinephrine	~80%
Adrenal hormone, norepinephrine	~20%
Simulated hemorrhage	500 mL
MAP, intact baroreflex	100 → 99 mmHg
Heart rate, intact baroreflex	77 → 106 /min
SVR, intact baroreflex	28.2 → 32.6 torr/L/min
MAP, no baroreflex	100 → 65 mmHg
Heart rate, no baroreflex	77 → 78 /min
SVR, no baroreflex	28.3 → 28.4 torr/L/min
1 torr	≈ 1 mmHg
Neural reflex turnaround	~1 s
Endocrine reflex onset	a minute or more
Endocrine reflex duration	hours to weeks
Baseline pump flow	5 L/min
Baseline mean arterial pressure	102 mmHg
Baseline CVP / right atrial pressure	2 mmHg
Mean systemic filling pressure	7 mmHg
Arterial pressure fall on arrest	95 mmHg
Venous pressure rise on arrest	5 mmHg
Venous to arterial compliance	~20 : 1
Pump at 1 L/min: arterial / venous	26 / 6 mmHg
Venous return curve linear up to	~7.5–8 L/min
Normal operating point	2 mmHg, 5 L/min
Moderate heart failure	~3 mmHg, 4 L/min
More volume, normal heart	~2.5 mmHg, >6 L/min

Distinctions that get mixed up¶

Pair	How to keep them apart
Nicotinic vs muscarinic	Both cholinergic. Nicotinic sits on the postganglionic neuron in both branches and on the adrenal medulla. Muscarinic sits on parasympathetic target tissue, M₂ at the SA and AV nodes.
Norepinephrine vs epinephrine receptors	Norepinephrine: alpha-1, alpha-2, beta-1. Epinephrine: alpha-1, beta-1, beta-2. Only epinephrine reaches beta-2.
Chronotropy vs dromotropy	Chronotropy is heart rate at the SA node. Dromotropy is conduction velocity through the AV node.
Vasoconstriction vs venoconstriction	Arteries: smaller radius, higher resistance. Veins: less volume and compliance, more pressure and venous return.
High-pressure vs low-pressure baroreceptors	Carotid sinus and aortic arch, stretch means pressure, CN IX and X. Atria, vena cavae, pulmonary vessels, right ventricle, stretch means volume, CN X only.
CVLM vs RVLM	Caudal inhibits, rostral drives sympathetic outflow. Baroreceptor firing activates the CVLM, which silences the RVLM.
Baroreflex vs Bainbridge reflex	Baroreflex defends arterial pressure and slows the heart when venous return rises. Bainbridge defends atrial filling and speeds it. Baroreflex dominates at low volume, Bainbridge at high volume.
Neural vs endocrine reflex	Neural: instant, short-lived, band-aid. Endocrine: delayed by a minute or more, lasts hours to weeks, often fixes the root cause.
Vasopressin vs aldosterone	Vasopressin retains water directly and vasoconstricts. Aldosterone retains sodium, and water follows osmotically.
Enzyme vs hormone in the renin-angiotensin system	Renin and ACE are enzymes (green). Angiotensin II, vasopressin, and aldosterone are hormones (blue). Angiotensinogen and angiotensin I are inactive.
ANP vs vasopressin	Same targets, vascular smooth muscle and kidney, opposite direction. ANP dilates and sheds water; vasopressin constricts and retains it.
Cardiac function curve vs Starling curve	Same x-axis idea, preload. Starling has stroke volume on y; the cardiac function curve has cardiac output.
Parallel shift vs slope shift	Volume or compliance: parallel, and mean systemic filling pressure moves. Resistance: slope pivots around a fixed mean systemic filling pressure.
Which axis is independent	Cardiac curve: right atrial pressure drives cardiac output. Venous return curve as built: venous return drives right atrial pressure. The axes are flipped only to superimpose them.

Check yourself¶

Compare parasympathetic and sympathetic pathways: neuron lengths, ganglion location, transmitter and receptor at each synapse.
Describe the sympathetic endocrine variation, including the hormone split and the receptors each hormone prefers.
For the SA node, AV node, myocardium, arteries, and veins, state which autonomic branches innervate each and the receptor and effect.
Explain how venoconstriction changes venous volume, pressure, compliance, venous return, and preload.
Using MAP = CO · SVR and R = 8ηl/(πr⁴), explain why vasoconstriction and vasodilation are primary determinants of afterload.
List the five ways sympathetic stimulation raises blood pressure and the way parasympathetic stimulation lowers it.
Why is baro a misnomer for baroreceptors?
Name the two arterial baroreceptor sites, the nerve serving each, and where their signals are integrated.
Describe how baroreceptor firing changes across a cardiac cycle as mean arterial pressure goes from extremely low to extremely high.
Trace the baroreflex response to a handstand, naming every medullary region and the effect on heart rate, contractility, and resistance.
Trace the response to standing up too quickly. What does it mean that the RVLM is disinhibited?
Why does the response to a sudden fall in pressure matter more than the response to a sudden rise?
In the 500 mL hemorrhage simulation, give the final MAP, heart rate, and SVR with and without the baroreflex, and explain the difference.
Where are the cardiopulmonary baroreceptors, and why is the right ventricle on the list?
List the integrating centers and effectors of the entire atrial stretch reflex.
Walk through the Bainbridge reflex for a rise in venous return and for a fall.
Give four situations that change venous return and the direction of each.
Explain respiratory sinus arrhythmia from thoracic volume and pressure through to heart rate.
Intravenous fluids raise venous return. Predict the heart rate response through each reflex, and explain which wins at low and at high blood volume.
Contrast neural and endocrine negative feedback on onset, duration, and what they fix.
Why do the endocrine loops correct both blood pressure and blood volume when the sensors detect volume?
Trace vasopressin from stimulus to its two effects, and say which effect is the band-aid and which fixes the root cause.
Name the two stimuli for renin release and how cardiopulmonary information reaches the kidney.
Walk from angiotensinogen to angiotensin II, naming each enzyme and where it acts, then list angiotensin II’s effects.
Explain where sodium goes, water follows, using aldosterone and ANP.
Describe the ANP reflex and why suppressing renin matters.
Classify heart rate, contractility, preload, and afterload as intrinsic or extrinsic, give an index for each, and name the one inversely related to cardiac output.
Explain the pump thought experiment: what happens to arterial and venous pressure on cardiac arrest, and why the changes are so unequal. Calculate the compliance ratio.
Define mean systemic filling pressure and locate it on the venous return curve before and after the axes are flipped.
Sketch how the venous return curve shifts with more blood volume, more compliance, vasodilation, and vasoconstriction.
Find the new operating point qualitatively for moderate heart failure, for added blood volume, and for both together.
Explain the two vascular curve shifts and the cardiac curve shift during strenuous exercise.