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60 Cards in this Set

  • Front
  • Back
Stroke volume (SV)
blood pumped/beat by each ventricle
Cardiac Output (CO)
Is volume of blood pumped/min by each ventricle
=SV x HR
Total blood volume is about 5.5L
chronotropic effect
influence HR
Autonomic innervation of SA node
Symp and Parasymp nerve fibers modify rate of spontaneous depolarization
NE and Epi -regulation of cardiac rate
stimulate opening of pacemaker HCN channels
This depolarizes SA faster, increasing HR
ACH - regulation of cardiac rate
promotes opening of K+ channels
The resultant K+ outflow counters Na+ influx, slowing depolarization and decreasing HR
Cardiac control center
located in medulla
coordinates activity of autonomic innervation
Total peripheral resistance (TPR)
impedance to blood flow in arteries
(regulates mean arterial pressure)= afterload which impedes ejection from ventricle
Contractility
strength of ventricular contraction
Ejection fraction
is SV/ EDV
Normally is 60%; useful clinical diagnostic tool
End diastolic volume (EDV)
volume of blood in ventricles at end of diastole
workload (preload) on heart prior to contraction
Frank-Starling Law of the Heart
States that strength of ventricular contraction varies directly with EDV
Is an intrinsic property of myocardium
As EDV increases, myocardium is stretched more, causing greater contraction and SV
sympathoadrenal
involving the sympathetic nervous system and the adrenal glands, especially increased sympathetic activity that causes increased secretion of epinephrine and norepinephrine.
Venous Return
Is return of blood to heart via veins
Controls EDV and thus SV and CO
Dependent on:
Blood volume and venous pressure
Vasoconstriction caused by Symp
Skeletal muscle pumps
Pressure drop during inhalation
capacitance vessels
term due to veins hold most of blood in body (~70%)
intracellular compartment
contains 2/3 of body H2O is inside cells
extracellular compartment
contains 1/3 total body H2O
80% of this is interstitial fluid; 20% is blood plasma
Net filtration pressure
hydrostatic pressure in capillary (17-37 mm Hg) - hydrostatic pressure of ECF (1 mm Hg)
colloid osmotic pressure
osmotic pressure exerted by proteins in blood plasma that usually tends to pull water into the circulatory system.
Starling forces
net filtration pressure and forces opposing it
Pc + pi (fluid out) - Pi + pp (fluid in)

Pc = Hydrostatic pressure in capillary
pi = Colloid osmotic pressure of interstitial fluid
Pi = Hydrostatic pressure in interstitial fluid
pp = Colloid osmotic pressure of blood plasma
Edema
excessive accumulation of ECF resulting from:
High blood pressure
Venous obstruction
Leakage of plasma proteins into ECF
Low plasma protein levels resulting from liver disease
Obstruction of lymphatic drainage
Myxedema
(excess production of glycoproteins in extracellular matrix) from hypothyroidism
can cause edema
glomerulus
part of kidney that filters plasma in urine
ADH (vasopressin)
released by Post Pit when osmoreceptors detect high osmolality
From excess salt intake or dehydration
Causes thirst
Stimulates H2O reabsorption from urine
inhibited by low osmolality
Aldosterone
Is steroid hormone secreted by adrenal cortex
Helps maintain blood volume and pressure through reabsorption and retention of salt and water
Release stimulated by salt deprivation, low blood volume, and pressure
angiotensin II
produced when there is a salt deficit, low blood volume, or low pressure
causes a number of effects all aimed at increasing blood pressure:
Vasoconstriction, aldosterone secretion, thirst
Atrial Natriuretic Peptide (ANP)
Expanded blood volume is detected by stretch receptors in left atrium and causes release of ANP
ANP inhibits aldosterone, promoting salt and water excretion to lower blood volume
And promotes vasodilation
ANP, together with decreased ADH, acts in a negative feedback system to lower blood volume
Physical Laws Describing Blood Flow
Flow rate is directly proportional to difference (DP = P1 - P2)
Flow rate is inversely proportional to resistance
Flow = DP/R
Poiseuille's Law
Blood flow = DPr^4(pi)
nL(8)
Resistance is directly proportional to length of vessel (L) and viscosity of blood (n)
Inversely proportional to 4th power of radius
the 2 major factors regulating blood flow
Mean arterial pressure and vascular resistance
total peripheral resistance
Sum of all vascular resistances within the systemic circulation
Extrinsic Regulation of Blood Flow
Sympathetic
Sympathoadrenal activation causes increased CO and resistance in periphery and viscera
Blood flow to skeletal muscles is increased
Because their arterioles dilate in response to Epi and their Symp fibers release ACh which also dilates their arterioles
Thus blood is shunted away from visceral and skin to muscles
Extrinsic Regulation of Blood Flow
Parasympathetic
Parasympathetic effects are vasodilative
However, Parasymp only innervates digestive tract, genitalia, and salivary glands
Thus Parasymp is not as important as Symp
Angiotenin II and ADH (at high levels) cause general vasoconstriction of vascular smooth muscle
Which increases resistance and BP
Nitric oxide (NO), bradykinin, prostacyclin
endothelium produces several paracrine regulators that promote relaxation:
NO
involved in setting resting “tone” of vessels
Levels are increased by Parasymp activity
Vasodilator drugs such as nitroglycerin or Viagra act
Endothelin 1
vasoconstrictor produced by endothelium
Myogenic control mechanisms
occur in some tissues because vascular smooth muscle contracts when stretched and relaxes when not stretched
matches blood flow to local tissue needs
Intrinsic Regulation of Blood Flow (Autoregulation)
Maintains fairly constant blood flow despite BP variation
active hyperemia
Low O2 or pH; or high CO2, adenosine, or K+ from high metabolism cause vasodilation which increases blood flow
Heart (and brain) must receive adequate blood supply at all times
Heart is most aerobic tissue--each myocardial cell is within 10 mm of capillary
Contains lots of mitochondria and aerobic enzymes
During systole the coronary vessels are occluded
Heart gets around this by having lots of myoglobin
]
Aerobic Requirements of the Heart
Regulation of Coronary Blood Flow
Blood flow to heart is affected by Symp activity
NE causes vasoconstriction (a effect); Epi causes vasodilation (b effect).
However, dilation accompanying exercise is due mostly to intrinsic regulation
Regulation of Blood Flow Through Skeletal Muscles
At rest, flow through skeletal muscles is low because of tonic sympathetic activity (via NE)
Flow through muscles is decreased during contraction because vessels are constricted
Circulatory Changes During Exercise
Symp activity causes vasodilation via Epi and local ACh release
Blood flow is shunted from periphery and visceral to active skeletal muscles
intrinsic regulation is major vasodilator
Symp effects cause SV and CO to increase
HR and ejection fraction also increases (vascular resistance goes down reducing afterload)
Cerebral Circulation
Gets about 15% of total resting CO
Held constant (750ml/min) over varying conditions
Is not normally influenced by sympathetic activity
myogenic regulation
When BP increases, cerebral arterioles constrict; when BP decreases, arterioles dilate
Cerebral Circulation 2
Regulated almost exclusively by intrinsic mechanisms
Arterioles dilate and constrict in response to changes in CO2 levels (leads to a drop in pH)
metabolic regulation
increases in local neural activity Arterioles are very sensitive to
Areas of brain with high metabolic activity receive most blood
thermoregulation
Skin blood flow is adjusted to keep body core temp at 37oC
By arterial dilation or constriction and activity of arteriovenous anastomoses which control blood flow through surface capillaries
Symp activity closes surface beds during cold and fight-or-flight, and opens them in heat and exercise
Blood Pressure (BP)
Arterioles play major role in control and distribution
contolled mainly by by HR, SV, and peripheral resistance
increase in these increases this
Sympathoadrenal activity raises BP via arteriole vasoconstriction and by increased CO
Kidney plays role in BP by regulating blood volume and thus stroke volume
baroreceptors
(stretch receptors) located in aortic arch and carotid sinuses
Increase in BP causes walls of these regions to stretch, increasing frequency of APs
send APs to vasomotor and cardiac control centers in medulla
Is most sensitive to decrease and sudden changes in BP
Atrial Stretch Receptors
Are activated by increased venous return and act to reduce BP
Stimulate reflex tachycardia (fast HR)
Inhibit ADH release (decreases blood volume) and promote secretion of ANP (decreases blood volume, antagonizes the vasoconstriction actions of angiotensin II)
auscultation
to examine by listening)
laminar flow
normal, quiet, smooth blood flow)
No sound is heard
Korotkoff sounds
sound is heard at pressure that blood is 1st able to pass thru cuff (= systolic pressure); last occurs when one can no long hear sound because cuff pressure = diastolic pressure
Pulse pressure
(systolic pressure) – (diastolic pressure)
Mean arterial pressure (MAP)
represents average arterial pressure during cardiac cycle
diastolic pressure + 1/3 pulse pressure
Hypertension
Blood pressure in excess of normal range for age and gender (> 140/90 mmHg)
Afflicts about 20% of adults
primary or essential hypertension
Increase in peripheral resistance is universal
CO and HR are elevated in many
Secretion of renin, Angio II, and aldosterone is variable
Sustained high stress (which increases Symp activity) and high salt intake act synergistically in development of hypertension
Prolonged high BP causes thickening of arterial walls, resulting in atherosclerosis
Kidneys appear to be unable to properly excrete Na+ and H2O
Secondary hypertension
caused by known disease processes
Treatment of Hypertension
Often includes lifestyle changes such as cessation of smoking, moderation in alcohol intake, weight reduction, exercise, reduced Na+ intake, increased K+ intake
Drug treatments include diuretics to reduce fluid volume, beta-blockers to decrease HR, calcium blockers, ACE inhibitors to inhibit formation of Angio II, and Angio II-receptor blockers
myoglobin
an O2 storage molecule that releases O2 to heart during systole