Cardiovascular Physiology 2 (9/18b) [Biomedical Sciences 1] Flashcards
What physical principles influence how blood flows through the system?
Pressure (P)
Flow (Q)
Resistance (R)
How are pressure, flow, and resistance related?
Q = ΔP / R
Q= flow (L/min) ΔP= pressure gradient (P1-P2) R= resistance
What factors affect resistance?
Viscosity
Vessel length
Vessel radius
Remember resistance ~ 1/radius^4
Pressure circuits in the CV system
Systemic system and pulmonary system
Pressure and resistance are much less in pulmonary circuit
Pulse pressure avg 80-120 mmHg
Pressures in the circuits
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
Cardiac Output equation
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
Pressure across the arterioles
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
Flow through one system is (less/greater/equal to) flow through the other system?
Equal to (=)
How does the vasculature regulate flow?
By regulating arteriole smooth muscle contraction since arterioles control how much blood an organ gets
Contraction = vasoconstriction Relaxation = vasodilation
Through local and distant mechanisms
Regulating Flow - Local Mechanisms
Tissue metabolites (dilation)
Myogenic (dilation/constriction)
Endothelial factors (dilation/constriction)
Local Mechanisms - Metabolites and Endothelial
Metabolites → Increase in blood flow in response to:
1) Active hyperemia
2) Reactive hyperemia
Active hyperemia
increase in tissue metabolic activity (exercise)
Tissue metabolism → release of metabolites → vasodilation
K+, phosphate, adenosine, prostaglandins, etc
Reactive hyperemia
period of occlusion
Shear of blood flow against vessel wall → releases vasodilator substance from endothelium → vasodilation
Local Mechanisms - Myogenic
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
Regulating Flow - Distant Mechanisms
Neural sympathetic (constriction)
Humoral (dilation/constriction)
Distant Mechanisms
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
Circulating catecholamines
epinephrine and norepinephrine flowing in the bloodstream
Baroreceptor Reflex (neural mechanism)
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
Renin-Angiotensin-Aldosterone System (humoral mechanism)
Key for LONG term management of BP
Decreased mean arterial pressure leads to decreased perfusion pressure in the kidneys
Increased release of renin
Renin
produced in kidneys, catalyzes angiotensinogen to angiotensin I
Angiotensin converting enzyme (ACE)
converts angiotensin I to angiotensin II (increase BP, vasoconstrictor)
3 Targets for Pharmacologic Management of Hypertension
Decrease cardiac output
Decrease total peripheral resistance
Decrease fluid volume
Pharmacologic Management of HTN - Decreased CO
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
Pharmacologic Management of HTN - Decreased TPR
Angiotensin converting enzyme (ACE) inhibitors
-Prevent formation of angiotensin II
Pharmacologic Management of HTN - Decreased Fluid Volume
Diuretics (furosemide)
-Increase production of urine by kidneys
Systemic circulation has ___ pressure gradient, while pulmonary circulation has ___ pressure gradient
High
Low
