Physiology 2: Cardiac

Question 1

Average MAP

Answer 1

~95 mmHg

Question 2

Define cardiac output (CO) and how do you calculate it?

Answer 2

CO = HR x SV

Question 3

Formula for MAP

Answer 3

MAP = CO x TPR

Question 4

Five basic components of the Reflex arc:

Answer 4

Receptors (bio-transducers)
Afferent pathways (nerves)
Central Integrator ("comparator", the CNS)
Efferent pathways (nerves or hormones)
Effector organ(s)

Question 5

Understand the baroreceptor reflex; is it a positive or negative feedback system?

Answer 5

Negative feedback system.
Decrease in MAP = Increase in Sympathetic and decrease in Parasympathetics. Results in increased HR, CO, and BP.
Increase in MAP = decrease in Sympathetic and increase in Parasympathetic. Results in decreased HR, CO, and BP.

Question 6

Know various atrial pressure control mechanisms, which are recruited when, degree of their effect.

Answer 6

Baroreceptors: rapid onset, fall off after several hours, large ability for pressure increase.
Renal - Blood volume pressure control: delay onset, massive ability for control at 1+ days.

Question 7

Baroreceptor Reflex Arc; components

Answer 7

1. Baroreceptors in carotid sinus, aortic arch and other large thoracic arteries. These receptors are tonically active.
2. Afferent pathways in cranial nerves IX and X
3. Medullary centers - comparison of MAP vs. baseline.
4. Efferent autonomics (symp and parasymp) pathways
5. Effector organs (heart, arterioles, and veins/venules, Adrenal Medulla)

Question 8

Carotid Sinus vs. Aortic Arch Baroreceptors

Answer 8

Carotid Sinus: most sensitive, threshold around 50-60 mmHg. Signal carried via CN IX (gossopharyngeal).
Aortic Arch: threshold around 100-110 mmHg (less sensitive). Afferents carried in CN X (Vagus).

Question 9

Baroreceptor activity; tonic vs. phasic

Answer 9

Tonic baroreceptor firing rate (static component) is dependent on the magnitude of MAP. Time average - # of responses over given time.
Phasic baroreceptor firing rate (dynamic component) reflects the rate of change of pressure, bursting pattern associated with rapid increase in BP.

Question 10

Baroreceptor adaptation

Answer 10

Capable of adaptation, typically seen in chronic hypertension. Results in a right shift of the response curve, can adjust back to the left over time.

Question 11

Pressor Center vs Depressor Center; control of vasomotor centers and peripheral vascular resistance

Answer 11

Pressor Center: when stimulated the pressor center is inhibited

• tonically active
• controls sympathetic outflow to peripheral vascular
• increase in afferent input (increased atrial pressure) results in decreased sympathetic output and passive vasodilation
• located in the lateral C-1 area

Depressor Center: when stimulated the depressor center inhibits the pressor center

• not tonically active
• appears to modulate the activity of the pressor center
• increase in afferent inputs (increased arterial pressure) results in an increase in depressor center output to the pressor center, a decrease in sympathetic outflow, and passive vasodilation
• located in medial A-1 area

Question 12

Cardioinhibitory and Cardiostiumlatory Centers

Answer 12

Cardioinhibitory center:

• tonically active
• controls the parasympathetic (vagus) output
• associated with the nucleus ambiguous
• increased afferent input (increased pressure) results in increased vagal output leading to a decrease in HR, decreased afferent input (decreased pressure) results in a decrease vagal output and increased HR

Cardiostimulatory center:

• tonically active
• controls the sympathetic output to the heart (SA and AV nodes and ventricular myocardium)
• increased afferent input decreases sympathetic outflow leading to decreased HR, contractility, and conduction velocity; decreased afferent input increases sympathetic outflow increasing HR, contractility, and CV.

Question 13

Sympathetic Nervous System (adrenergic receptors)

Answer 13

A1 receptors: vascular smooth muscle, causes vasoconstriction and venoconstriction.

B1 Receptors: respond to sympathetically released norepi and circulating norepi and epinephrine.

• Heart: increased contractility (+ inotropic), increased heart rate (+ chronotropic), increased rate of conduction (+ dromotropic).
• Kidneys: released of renin - induces renin-angiotensin-aldosterone cascade in response to decreased effective circulating blood volume.

Question 14

Parasympathetic Nervous System (cholinergic receptors)

Answer 14

Vagus Nerve: preganglionic parasympathetic innervation, goes to SA node, decreases HR (- chronotropic). Also some innervation to the AV node to slow conduction velocity (-domotropic).

Cranio-sacral outflow: vasodilation in vascular smooth muscle in response to release of postganglionic acetylcholine.

Endothelial cells: possess muscarinic receptors the cause relaxation via release of NO and/or other endothelial-derived factors.

Cholinergic sympathetic nerve fibers: act via muscarinic and medial transient vasodilation of skeletal muscle. NOT involved in regulation of BP.

Question 15

Which vessels have the greatest drop in arterial pressure?

Answer 15

Small arterioles

Question 16

Vascular tone

Answer 16

Arterioles possess an intrinsic level of basal or myogenic tone, independent of of neural or humoral influences.

• Increases in the activity of vasoconstrictor stimuli cause ACTIVE VASOCONSTRICTION, while a decrease in active tone results in PASSIVE VASODILATION.
• ACTIVE VASODILATION occurs in response to a vasodilatory influence and results in decreased vascular resistance below basal tone. PASSIVE VASOCONSTRICTION occurs when the dilatory influence is removed and arterial tone returns to basal level.

Question 17

Myogenic activity as a mechanism of autoregulation of peripheral vascular blood flow

Answer 17

• The rapid stretch of vascular smooth muscle causes it to contract, resulting in a decrease in vessel lumen diameter and increases flow resistance; this is myogenic vasoconstriction.
• This myogenic response of vascular smooth muscle to changes in wall tension is an intrinsic function of smooth muscle itself.
• The myogenic response is important in protecting the capillaries from sudden increases in blood pressure.

Question 18

Metabolic vasodilatation as a mechanism of autoregulation of peripheral vascular blood flow

Answer 18

• An increase in tissue metabolism cause the release of substances in the tissues that relax vascular smooth muscle and produces metabolic vasodilation (vasoregulation).
• Metabolic vasodilation increases tissue blood flow and the delivery of oxygen and substrates, as well as the removal of metabolic waste products, in proportion to tissue metabolism.

Question 19

What are autocoids and what is their function?

Answer 19

Autocoids are locally produced vasoactive substances and are generally potent vasodilators. No single substance has been shown to account for the full magnitude of the local response, felt that they likely act in a synergistic manner.

Question 20

Intrinsic Neurons; function, role

Answer 20

Found in the walls of arteries and arterioles, may be involved in in rapid local changes in tissue blood flow. Nerves may be involved in transmission of excitation and/or inhibition along vessel segments.

Question 21

Tissue pressure theory; function, role

Answer 21

NOT true autoregulation. High perfusion pressure and flow to encapsulated organs can lead to excessive fluid filtration and edema formation which can lead to increased tissue pressures. An increase in tissue pressure can compress the blood vessels and reduce blood flow (Pout > Pin).

Question 22

Reactive hyperemia

Answer 22

When flow to a tissue is restored after a period of ischemia, flow increases exceeds the pre-ischemic levels. The magnitude and duration the reactive hyperemia are directly correlated to the duration of the ischemic period.

Question 23

Active hyperemia

Answer 23

• During periods of increased tissue metabolic activity the rate of substrate utilization and metabolic waste production increases dramatically. Coincident with the increased metabolic activity is an increase in local blood flow. This active hyperemia is observed even in the absence of extrinsic control mechanisms. Overrides sympathetic input in some instances.
• This is an example of metabolic vasoregulation.