Lecture 6 (RAAS and Hemodynamics) Flashcards
Function of Renin:
necessary for angiotensin II synthesis
Function of Angiotensin II:
- vasoconstrictor
- stimulates aldosterone secretion from adrenal cortex
Function of Aldosterone:
- promotes Na+ conservation by kidneys; H2O follows Na+
- increases intravascular volume
- vasoconstrictor
All angiotensin II bioactivity in vascular smooth muscle and cardiac muscle is mediated by what receptor?
AT1
Actions of angiotensin II that lead to increased blood pressure (4):
- vasoconstriction
- block in high pressure baroreceptor activity
- increased aldosterone levels
- stimulation of norepi release from post-ganglionic SNS fibers
Angiotensin II can block high pressure baroreceptor input. How does this cause an increase in BP?
- endogenous counter-response to elevated BP is neutralized.
- SNS not shut off in response to elevated BP.
- SNS has free-reign to maintain increased BP.
Where are receptors for RAAS (angiotensin II and aldosterone) located?
- myocardium
- vascular smooth muscle
- kidney
Effect of RAAS (aldosterone and angiotensin II) on the heart:
- contributes to left ventricular hypertrophy
- increased wall stress and oxygen demand
- reduced ejection fraction
Effect of RAAS (aldosterone and angiotensin II) on vascular smooth muscle:
- leads to tunica intima and tunica media thickening
- can cause vascular stenosis
Effect of RAAS (aldosterone and angiotensin II) on the kidney:
- impairs normal renal function
- can lead to renal failure.
Treatments for hypertension:
- ACE inhibitors (angiotensin II)
- ARBs (AT1 receptors)
- Diuretics (aldosterone)
- Calcium channel blockers (amlodipine)
- beta-blockers (SNS)
Function of verapamil and cardizem:
- blocks Type L calcium channels in the heart.
- help reduce heart rate by increasing AV nodal delay.
Function of amlodipine:
- blocks Type L calcium channels in vascular smooth muscle.
- prevents vasoconstriction.
Primary hypertension:
- hypertension due to an unknown cause.
- treatable with general hypertension protocol.
- ACE inhibitors, ARBs, calcium channel blockers, etc.
Secondary hypertension:
- hypertension due to another medical condition.
- not treatable with general hypertension protocol.
How, specifically, does using a beta-blocker decrease blood pressure?
- beta-blockers block SNS effects on the heart.
- decrease HR and inotropy, and therefore CO.
- CO = SV x HR.
- MAP = CO X TPR.
General primary hypertension treatment protocol:
-
First:
- thiazide diuretic
-
Second:
- thiazide diuretic + ACE inhibitor/ARB
-
Third:
- thiazide diuretic + ACE inhibitor/ARB + Ca2+ channel antagonist
The four body systems involved in hypertension, and drugs that target their function:
-
cardiac
- calcium channel blockers, beta-blockers
-
renal
- diuretics, ACE inhibitors, ARBs
-
vascular smooth muscle
- calcium channel blockers, ACE inhibitors, ARBs, alpha-1 receptor blockers
-
ANS
- beta-blockers
Blood vessels with the highest velocity and lowest velocity of flow:
- highest velocity: aorta
- lowest velocity: capillaries
Blood vessels with the highest and lowest total cross-sectional area:
- highest: capillaries
- lowest: aorta
Blood vessels with the highest and lowest transmural (wall) pressure:
- highest: aorta
- lowest: vena cava
Total peripheral resistance equation:
-
TPR = (Pa - Pv)/Qt.
- Qt = cardiac output (CO = SV x HR).
- Pa - Pv = CO x R
60% of total peripheral resistance is due to:
- arteriolar resistance
- Arterioles can undergo 4x changes in lumen diameter, which leads to up to a 256x change in conductance.
Which blood vessel has the greatest influence over total peripheral resistance?
arterioles
Peak arterial pressure occurs at:
- the end of decreased/slow systolic ejection phase, which is the end of the T wave.
Lowest arterial pressure occurs at:
- the end of isovolumetric contraction.
- immediately before the aortic valve opens
Draw ECG with arterial pressure graph underneath:
Where does systolic pressure normalize with diastolic pressure?
- right before entering the capillaries after traveling through the arterioles.
How do arterioles maintain a relatively constant capillary pressure?
- by adjusting resistance to flow with precapillary sphincters.
-
ΔP = Q x R
- flow (Q) and capillary pressure remain relatively constant, so arterioles adjust arterial pressure going into capillaries via resistance.
The four Starling forces governing capillary filtration/exchange with the interstitial fluid:
- Capillary hydrostatic pressure
- Capillary oncotic pressure
- Interstitial fluid hydrostatic pressure
- Interstitial fluid oncotic pressure
What is oncotic pressure, and how does it affect capillary filtration?
- The tendency for fluids to be pulled toward proteins.
- Albumin generates about 70% of the oncotic pressure in capillaries, which decreases capillary filtration into interstitial fluid.
On what end of capillaries is filtration the greatest?
- arteriole
- Pcap > Pif; filtration occurs
- πif > πcap; filtration occurs
Draw a capillary with starling force magnitudes:
What carries capillary filtrate in the interstitial fluid back to the venous system?
- lymphatic ducts
Lymphatic function is compromised if the amount of capillary filtrate in the interstitial fluid is greatly increased. This causes edema. How can this occur?
- increased arterial pressure (increased Pcap)
- increased venous pressure (increased Pcap)
- a pathological increase in capillary permeability
When does edema occur?
- when there is increased capillary pressure that leads to increased filtration that overwhelms the lymphatic system.
The two types of diffusion that occurs from capillaries to interstitial fluid:
-
via pores:
- water soluble molecules; rapid
-
via plasma membrane:
- lipid-soluble molecules (gases); very rapid
The pressure drop across the arterial-venous tree is determined by what equation?
Pa - Pv = CO x R
- R is determined by the arterial side, mostly by arterioles.
(TPR = (Pa - Pv)/QT)
