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12 Cards in this Set

  • Front
  • Back
What is arterial pulse pressure?
Arterial pulse pressure is the difference between systolic and diastolic arterial pressure.
Name the three parameters that determine systemic blood pressure:
1) Cardiac output (heart rate x stroke volume)

2) Peripheral resistance

3) Blood volume
Describe the renin-angiotensin-aldosterone (RAAD) system. How does this system alter blood pressure?
When juxtaglomerular cells in the kidney sense low blood pressure they release renin. Renin converts angiotensinogen to angiotensin I. Angiotensin I, in turn, is converted by angiotensin converting enzyme (ACE) to angiotensin II. Angiotensin II is a potent vasoconstrictor and increases blood pressure by increasing peripheral resistance. Additionally, angiotensin II induces the renal cortices to release aldosterone from the zona glomerulosa.
Aldosterone promotes reaborption of Na+ in the kidney and thus increases blood pressure by increasing blood volume.
Describe the effect of each on heart rate and how the effect is achieved:
1) Sympathetic impulses
2) Parasympathetic impulses
Now, describe the effect of each on contractility and how the effect is achieved:
3) Sympathetic impulses
4) Parasympathetic impulses
1) Sympathetic impulses (via cardiac accelerator nerves and beta-1 adrenergic receptors) increase heart rate by increasing the amount of open Na+ pacemaker channels
2) Parasympathetic impulses (via vagus nerve and muscarinic cholinergic receptors) decrease heart rate by decreasing the amount of open Na+ pacemaker channels
3) Sympathetic impulses increase contractility by enhancing influx of Ca++ through L-type channels
4) Parasympathetic impulses have little effect on contractility because there are few cholinergic receptors in the myocardium outside the pacemaker cells
Where are the carotid sinuses located?
The carotid sinuses are small widenings of the right and left INTERNAL carotid arteries located just distal the point where the common carotid bifurcates.
Describe the carotid sinus reflex:
Baroreceptors in the carotid sinus send impulses to the cardiovascular center via the glossopharyngeal nerves (CN IX). If blood pressure is too high, the baroreceptors send these impulses at a faster rate and the cardiovascular center responds by DECREASING sympathetic impulses to the heart and INCREASING parasympathetic impulses to the heart, thereby decreasing heart rate and contractility.
Conversely, if pressure in the carotid sinuses is too low the baroreceptors send impulses at a slower rate and the cardiovascular centre responds by INCREASING sympathetic impulses and DECREASING parasympathetic impulses to the heart, thereby increasing heart rate and contractility.
Sympathetic impulses are carried from the cardiovascular center to the heart via the cardiac accelerator nerves, while parasympathetic impulses are carried via the vagus nerve (CN X).
Overall effect of high blood pressure in carotid sinuses:
Decreased sympathetic activity (decreased heart rate, contractility)
Increased parasympathetic activity (decreased heart rate)
Overall effect of low blood pressure in carotid sinuses:
Increased sympathetic activity (increased heart rate and contractility)
Decreased parasympathetic activity (increased heart rate)
Baroreceptors in the carotid sinuses carry impulses to the cardiovascular center via which cranial nerve?
Glossopharyngeal nerve (CN IX)
Describe the aortic reflex:
Baroreceptors in the aortic arch send impulses to the cardiovascular center via the vagus nerve (CN X). If blood pressure is too high, the baroreceptors send these impulses at a faster rate and the cardiovascular center responds by DECREASING sympathetic impulses to the heart and INCREASING parasympathetic impulses to the heart, thereby decreasing heart rate and contractility.
Conversely, if pressure in the aortic arch is too low the baroreceptors send impulses at a slower rate and the cardiovascular centre responds by INCREASING sympathetic impulses and DECREASING parasympathetic impulses to the heart, thereby increasing heart rate and contractility.
Sympathetic impulses are carried from the cardiovascular center to the heart via the cardiac accelerator nerves, while parasympathetic impulses are carried via the vagus nerve (CN X).
Overall effect of high blood pressure in aortic arch:
Decreased sympathetic activity (decreased heart rate, contractility)
Increased parasympathetic activity (decreased heart rate)
Overall effect of low blood pressure in aortic arch:
Increased sympathetic activity (increased heart rate and contractility)
Decreased parasympathetic activity (increased heart rate)
Baroreceptors in the aortic arch send impulses to the cardiovascular center via which cranial nerve?
Vagus nerve (CN X)
Explain how carotid sinus massage can slow heart rate:
The technique of carotid sinus massage relies on the carotid sinus reflex. The massage increases pressure in the carotid sinus. Baroreceptors there report the increase in pressure to the cardiovascular center via CN IX. The cardiovascular center, decreases sympathetic impulses and increases parasympathetic impulses to the heart, slowing heart rate and dropping contractility.
Describe the mechanism of action of aldosterone:
Aldosterone binds to receptors on the principal cells of the collecting duct, stimulating them to reabsorb more Na+.

The exact mechanism of action is unknown, but it is postulated that aldosterone either ramps up the activity of the Na+/K+ pump directly or up-regulates proteins for apical Na+ channels.

In other words, aldosterone increases blood pressure by increasing blood volume. It increases blood volume (ECFV) by increasing total body Na+.
Why does hypercortisolemia cause hypertension?
Glucocorticoids can bind to the aldosterone receptors on the collecting ducts of the principal cells, thereby enhancing Na+ reabsorption and a subsequent increase in blood volume.