Cardiovascular Physiology 2 (9/18b) [Biomedical Sciences 1] Flashcards

1
Q

What physical principles influence how blood flows through the system?

A

Pressure (P)
Flow (Q)
Resistance (R)

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2
Q

How are pressure, flow, and resistance related?

A

Q = ΔP / R

Q= flow (L/min)
ΔP= pressure gradient (P1-P2)
R= resistance
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3
Q

What factors affect resistance?

A

Viscosity
Vessel length
Vessel radius

Remember resistance ~ 1/radius^4

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4
Q

Pressure circuits in the CV system

A

Systemic system and pulmonary system

Pressure and resistance are much less in pulmonary circuit

Pulse pressure avg 80-120 mmHg

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5
Q

Pressures in the circuits

A

Large arteries: systemic 90-100 mmHg, pulmonary 15 mmHg

Arterioles: systemic 50 mmHg, pulmonary n/a

Capillaries: systemic 20 mmHg, pulmonary 10 mmHg

Large vein: systemic 4 mmHg, pulmonary 8 mmHg

Atrium: systemic 0-2 mmHg, pulmonary 2-5 mmHg

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6
Q

Cardiac Output equation

A

CO = BP / TPR

CO = cardiac output (L/min)
BP = blood pressure (mmHg)
TPR = total peripheral resistance

(Similar to Q = ΔP / R)

Rearrange to get BP = CO * TPR

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7
Q

Pressure across the arterioles

A

Arterioles are the greatest source of resistance to flow in the cardiovascular system and a key determinant of TPR

Biggest pressure drop happens (~50 mmHg drop) across arterioles

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8
Q

Flow through one system is (less/greater/equal to) flow through the other system?

A

Equal to (=)

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9
Q

How does the vasculature regulate flow?

A

By regulating arteriole smooth muscle contraction since arterioles control how much blood an organ gets

Contraction = vasoconstriction
Relaxation = vasodilation

Through local and distant mechanisms

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10
Q

Regulating Flow - Local Mechanisms

A

Tissue metabolites (dilation)

Myogenic (dilation/constriction)

Endothelial 
factors (dilation/constriction)
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11
Q

Local Mechanisms - Metabolites and Endothelial

A

Metabolites → Increase in blood flow in response to:

1) Active hyperemia
2) Reactive hyperemia

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12
Q

Active hyperemia

A

increase in tissue metabolic activity (exercise)

Tissue metabolism → release of metabolites → vasodilation
K+, phosphate, adenosine, prostaglandins, etc

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13
Q

Reactive hyperemia

A

period of occlusion

Shear of blood flow against vessel wall → releases vasodilator substance from endothelium → vasodilation

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14
Q

Local Mechanisms - Myogenic

A

Autoregulation - intrinsic property of vascular smooth muscle allows the vessel to adjust diameter to maintain constant flow despite changes in BP

Dilates to maintain flow in response to decrease BP

Constricts to maintain flow in response to increase BP

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15
Q

Regulating Flow - Distant Mechanisms

A

Neural sympathetic (constriction)

Humoral (dilation/constriction)

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16
Q

Distant Mechanisms

A

Blood vessels innervated by sympathetic nervous system
-Norepinephrine acts on alpha-1 receptors → vasoconstriction

SNS also stimulates adrenal cortex
-Releases epinephrine into bloodstream (circulating catecholamines)

Kidneys release hormones that regulate vessel contractions and resistance
-Important for long term maintenance of BP

17
Q

Circulating catecholamines

A

epinephrine and norepinephrine flowing in the bloodstream

18
Q

Baroreceptor Reflex (neural mechanism)

A

Key for SHORT term management of BP

Sensors detect change in pressure, processor develops response, effector carries out response

If arterial pressure decreases

1) increase cardiac output
- Parasympathetic withdrawal → increased HR
- Sympathetic activity → increased HR, increased SV

2) increase TPR via sympathetically-mediated vasoconstriction
3) Sympathetic constriction of veins to increase venous return

19
Q

Renin-Angiotensin-Aldosterone System (humoral mechanism)

A

Key for LONG term management of BP

Decreased mean arterial pressure leads to decreased perfusion pressure in the kidneys

Increased release of renin

20
Q

Renin

A

produced in kidneys, catalyzes angiotensinogen to angiotensin I

21
Q

Angiotensin converting enzyme (ACE)

A

converts angiotensin I to angiotensin II (increase BP, vasoconstrictor)

22
Q

3 Targets for Pharmacologic Management of Hypertension

A

Decrease cardiac output

Decrease total peripheral resistance

Decrease fluid volume

23
Q

Pharmacologic Management of HTN - Decreased CO

A

Calcium channel blockers (diltiazem)
-Block influx of Ca2+ during plateau of cardiac action potential, thereby decreasing cardiac contractility and SV

Beta blockers (propranolol)
-Block SNS stimulation of HR and SV, leading to decreased CO
24
Q

Pharmacologic Management of HTN - Decreased TPR

A

Angiotensin converting enzyme (ACE) inhibitors

-Prevent formation of angiotensin II

25
Q

Pharmacologic Management of HTN - Decreased Fluid Volume

A

Diuretics (furosemide)

-Increase production of urine by kidneys

26
Q

Systemic circulation has ___ pressure gradient, while pulmonary circulation has ___ pressure gradient

A

High

Low