Costanzo-Cardiovascular Physiology
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| atrioventricular (AV) valves | one-way valves connecting atrium=>ventricle
tricuspid valve (right heart)
mitral valve (left heart)
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| systemic circulation | left heart, systemic arteries, capillaries, veins
left ventricle pumps blood to all organs except lungs
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| pulmonary circulation | right heart, pulmonary arteries, capillaries, veins
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| cardiac output | rate blood pumped out from either ventricle per unit time
CO=SV x HR
in steady state right heart CO= left heart CO
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| venous return | rate blood returned to atria from veins
in steady state CO=venous return
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| circuitry | LV=>aorta=>organs=>veins=>RA=>RV=>pulmonary artery=>lungs=>pulmonary vein=>LA=>LV
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| semilunar valve | pulmonic valve (right heart)
aortic valve (left heart)
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| arteries | functions to deliver oxygenated blood to organs
thick-walled-->receive high pressure blood (stressed volume)
extensive elastic tissue, smooth muscle, connective tissue
aorta the largest artery-->medium and small-sized arteries branch from it
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| arterioles | smallest branches of arteries
site of highest resistance to blood flow=>can be changed by alteration of SNS activity, circulating catecholamines, vasoactive substances
contains alpha1-adrenergic and beta2-adrenergic receptors
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| alpha1-adrenergic receptors | commonly found in several vascular beds-->constricts smooth muscle-->increases resistance to blood flow
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| beta2-adrenergic receptors | found in arterioles of skeletal muscle=>dilates sooth muscle=>↓ resistance to blood flow
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| capillaries | thin-walled structures lined with single layer of endothelial cells surrounded by basal lamina
not all perfused with blood with blood all the time=>depends on metabolic needs
site of exchange
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| veins and venules | thin-walled structures with endothelial cell layer surrounded by basal lamina
very large capacitance=>capacitance changes with contraction of smooth muscle
holds largest % of blood=>unstressed vol (low press)
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| velocity of blood flow | v=Q/A
highest in aorta
lowest in capillaries
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| pressure difference | driving force for blood flow
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| resistance | impediment to flow
major mechanism to change blood flow thru changing blood vessel resistance in arterioles
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| blood flow | Q=(delta)P/R
used to measure TPR and resistance in single organ
direction of blood flow always from high to low
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| total peripheral resistance (TPR) | total resistance of entire systemic vasculature
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| Poiseuille equation | R=8nl/(3.14r^4)
factors that determine resistance of blood flow
R=resistance
n=viscosity of blood
l=length of blood vessel
r^4=radius of blood vessel
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| series resistance | total resistance= to sum of individual resistances
total flow thru each level the same
press ↓ progressively as blood flows thru each sequential component
arrangement of blood vessels within an organ
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| parallel resistance | total resistance less than any individual resistance=>adding more resistance ↓ total resistance
*increasing one individual resistance ↑ total resistance
no loss of press in major arteries
seen in aortic branching
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| laminar flow | streamlined blood flow=>parabolic profile=>velocity highest at center and lowest toward vessel walls
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| turbulent flow | lamina flow disrupted to streams mixing radially and axially=>seen in valves or sites with blood clots
more energy required to drive flow
often accompanied by murmurs
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| Reynold's number | used to predict laminar or turbulent flow
<2000 laminar
>3000 turbulent
NR=pdv/n
NR=Reynold's number
p=density of blood
d=diameter of blood vessel
v=velocity of blood flow*
n=viscosity of blood*
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| anemia and Reynold's number | ↑ Reynold's number due to
1)↓ blood viscosity
2)high CO
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| thrombi and Reynold's number | ↑ Reynold's number
1)narrows blood vessel diameter
2)↑ blood velocity at site of thrombus
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| capacitance | describes vol of blood a vessel can hold at a given press
C=V/P
C=compliance
V=volume
P=pressure
higher compliance=>more vol it can hold at given press
veins most compliant and contain unstressed vol
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| changes in compliance of veins | leads to redistribution of blood between veins and arteries
↑ compliance shifts blood from arteries=>veins
↓ compliance shifts blood from veins=>arteries
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| compliance of arteries and aging | walls get stiffer, less distensible, less compliant
arteries hold less blood=>why elderly have higher BP
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| pressures in cardiovascular system-systemic | aorta=100
large arteries=100(120/80)
arerioles=50
capillaries=20
vena cava=4
right atrium=0-2
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| pressures in cardiovascular system-pulmonary | pulmonary artery=15(25/8)
capillaries=10
pulmonary vein=8
left atrium=2-5
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| aorta and BP | largest artery=>medium and small-sized arteries branch from it
mean press very high
1)large vol pump from left ventricle into aorta
2)low compliance of arterial wall
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| large arteries and BP | high mean press because high elastic recoil of arterial walls
pulsations greater here than aorta=>higher systole and lower diastole
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| small arteries and BP | where arterial press begins to ↓
pulse press ↓ in small arteries and absent in arterioles
most significant ↓ in arterioles because has highest resistance to flow
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| capillaries and BP | press ↓ further from arterioles
1)frictional resistance to flow
2)filtration of fluid
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| venules and veins and BP | press ↓ further from capillaries because compliance is very high
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| pulsations | reflect pulsatile activity of heart: ejecting blood during systole=>resting dring diastole=>ejecting blood=>resting
each pulsatile cycle coincides with one cardiac cycle
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| diastolic pressure | lowest arterial press measured during cardiac cycle
press in artery during ventricular relaxation=>no blood being ejected from left ventricle
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| systolic pressure | highest arterial press measured during cardiac cycle
press in artery after blood ejected from left ventricle during systole
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| dicrotic notch | "blip" in arterial press curve produced when aortic valve closes=>produces brief period of retrograde flow=>↓ aortic press below systolic value
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| pulse pressure | difference between systolic and diastolic press=>magnitude reflects SV
will change if SV changes
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| stroke volume | vol of blood ejected from left ventricle on a single beat
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| mean arterial pressure (MAP) | average press in a complete cardiac cycle=>the driving force for blood flow in arteries
MAP=diastolic press + 1/3 pulse press
*diastolic press used because greater fraction of each cardiac cycle spent in diastole than systole
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| dampening of pulse pressure | 1)resistance of blood vessels=>particularly arterioles
2)compliance of blood vessels=>particularly veins
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| arteriosclerosis | plaque deposits in arterial walls ↓ diameter of arteries=>makes them stiffer and less compliant
↓ compliance=>SV prod greater ∆ in arterial press
↑ systolic press, pulse press, and mean press
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| aortic stenosis | aortic valve is narrowed
SV ↓=>less blood enters aorta
↓ systolic press, pulse press, and mean arterial press
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| aortic regurgitation | when aortic valve incompetent=>one-way flow disrupted
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| contractile cells | working cells of heart=>majority of atrial and ventricular tissues
AP in these cells lead to contraction and generation of force or press
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| conducting cells | constitute tissues of SA node, atrial internodal tracts, AV node, bundle of His, and Purkinje system
specialized muscle cells=>function to rapidly spread AP over entire myocardium
*can generate AP spontaneously=>normally suppressed except for SA n
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| SA node | serves as pacemaker
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| spread of excitation within heart | SA node=>atrial internodal tracts=>atria=>AV node=>bundle of His=>Purkinje system=>ventricles
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| AV node | slow conduction here ensures ventricles have sufficient time to fill with blood before they are activated and contract
↑ conduction leads to ↓
1)ventricular filling
2)SV
3)cardiac output
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| His-Purkinje system | conduction is extremely fast=>rapidly distributes AP to ventricles=>important for efficient contraction and ejection of blood
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| normal sinus rhythm | pattern and timing of electrical activation of heart normal
1)AP must originate in SA node
2)SA nodal impulses must be regular (60-100 per min)
3)activation of myocardium must occur in correct sequence, timing, and delays
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| resting membrane potential | determined primarily by K+ in cardiac cells=>conductance to K+ at rest is high=>resting membrane potential close to K+ equilibrium potential
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| AP basis for ventricles, atria, and Purkinje system | 1)long duration=>long refractory period
2)stable resting membrane potential
3)plateau=>sustained period of depolarization=>explains long duration of AP and refractory period
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| phases of AP for ventricles, atria, and Purkinje system | 1)phase 0, upstroke
2)phase 1, initial depolarization
3)phase 2, plateau
4)phase 3, repolarization
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| AP-phase 0 | upstroke=>rapid depolarization by transient ↑ in Na+ conductance (inward current)
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| AP-phase 1 | initial depolarization=>brief period of repolarization from inactivation of Na+ channels and outward K+ current
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| AP-phase 2 | plateau=>long period of stable, depolarized membrane potential
result of ↑ in Ca2+ conductance=>slow inward current of Ca2+ through L-type channels
balanced by outward K+ current
*initiates Ca2+-induced Ca2+ release
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| AP-phase 3 | repolarization=>begins gradually then rapidly with ↑ outward K+ current and ↓ Ca2+ inward current
outward K+ current ↓ as membrane potential fully repolarizes
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| AP-phase 4 | resting membrane potential=>membrane potential stable again
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| L-type channels | inhibited by Ca2+ channel blockers=>nifedipine, diltiazem, verapamil
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| AP in SA node | 1)phase 0, upstroke
2)phase 3, repolarization
3)phase 4, spontaneous depolarization
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| SA node AP-phase 0 | upstroke=>result of ↑ in Ca2+ conductance and inward current thru T-type Ca2+ c hannels
*upstroke not as sharp as in ventricules, atria, and Purkinje upstroke
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| SA node AP-phase 3 | repolarization=>from ↑ in K+ conductance and outward K+ current
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| SA node AP-phase 4 | spontaneous depolarization=>from "funny" inward Na+ current turned on by previous repolarization=>ensures each AP in SA node followed by another AP
longest portion of SA node AP
rate of this phase sets heart rate
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| latent pacemakers | myocardial cells other than SA node that have intrinsic automaticity
AV node, bundle of His, and Purkinje fibers=>not expressed due to overdrive suppression
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| overdrive suppression | suppression of latent pacemakers by driving their heart rate
ex)when SA node drives heart rate
fastest potential pacemaker set the heart rate=>suppresses other by driving their firing rate
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| ectopic pacemaker | latent pacemakers that become the pacemaker
occurs when 1) SA node suppressed or 2)conduction of its AP blocked or 3)latent pacemaker faster than SA node
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| firing rate of SA node and latent pacemakers | SA node=70-80
AV node=40-60
Bundle of His=40
Purkinje fibers=15-20
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| AV delay | conduction velocity slowest in AV node=>ensures ventricles have time to fill with blood from atria
requires approx. 1/2 total conduction time through myocardium
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| conduction velocity | speed AP propagates thru tissue
depends on size of inward current during upstroke and cable properties (gap junctions)
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| excitability | capacity of myocardial cells to generate AP in response to inward depolarizing current
*amount of inward current require to bring myocardial site to threshold potential
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| refractory period | when no upstroke can occur due to closed inactivation gates=>no upstroke no AP
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| absolute refractory period | cell completely refractory to fire another AP=>incapable of generating a 2nd AP no matter how large the stimulus
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| effective refractory period | 2nd AP can be generated a conducted AP cannot be generated
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| relative refractory period | 2nd AP can be generated with a stimulus greater-than-normal but will have
1)abnormal configuration
2)shortened plateau phase
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| supranormal period | cell more excitable than normal during this period=>less inward current required to depolarize cell to threshold potential
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| chronotropic effects | effects of ANS on heart rate
sympathetic stimulation ↑ heart rate
parasympathetic stimulation ↓ heart rate
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| positive chronotropic effects | ↑ heart rate=>SNS stimulate beta1 receptors in SA node=>↑ conduction of "funny" channels=>↑ phase 4 depolarization
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| negative chronotropic effects | ↓ heart rate=>PNS stimulates M2 receptors in SA node
1)↓ conduction of "funny" channels=>↓ phase 4 depolarization
2)↑ conductance of K+-Ach channel=>enhances outward K+ current=>hyperpolarizes SA nodal cells
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| dromotropic effects | effects of ANS on conduction velocity
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| positive dromotropic effects | SNS ↑ conduction velocity thru AV node=>↑ rate AP conducted from atria to ventricles
mechanism thru ↑ Ca2+ conduction and inward current
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| negative dromotropic effects | PNS ↓ conduction velocity thru AV node=>↓ rate AP conducted from atria to ventricles
1)↓ Ca2+ conduction and inward current
2)↑ conduction of K+-Ach channel and outward K+ current
can produce heart block
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| heart block | AP potentials not conducted at all from atria to ventricles
different degrees where conduction is slowed or severe cases where AP not conducted to ventricles at all
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| ECG- P wave | depolarizaton of atria
duration correlates with conduction time thru atria
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| ECG- PR interval | time from initial depolarizatoin of atria to initial depolarization of ventricles
includes P wave and PR segment
PR segment and interval corresponds to AV node conduction
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| ECG- QRS complex | represents depolarization of ventricles
short duration because conduction velocity takes place in His-Purkinje system
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| ECG- T wave | repolarization of ventricles
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| ECG- QT interval | represents first ventricular depolarization to last ventricular repolarization
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| ECG- ST segment | part of QT interval=>correlates with plateau of ventricular AP
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| ECG- heart rate | number of QRS complexes
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| ECG- cycle length | R-R interval
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| arrhythmias | abnormal heart rhythms
↑ heart rate a factor
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| myocardial cell structure | composed of sarcomeres
thick filaments composed of myosin
thin filaments composed of actin, tropomyosin, and troponin
contraction thru sliding filament model
contains T tubules (continuous with cell membrane) and sarcoplasmic reticulum
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| actin | globular protein with myosin-binding site
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| tropomyosin | runs along groove of twisted actin strands and blocks myosin-binding site
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| troponin | globular complex of 3 subunits=>troponin C subunit binds Ca2+ and changes conformationally to remove tropomyosin from myosin-binding site
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| Ca2+ release from sarcoplasmic reticulum | determined by
1)amount of Ca2+ previously stored
2)size of inward Ca2+ current during plateau of action potential
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| cross-bridges | formed between actin and myosin during contraction to produce tension
cross-bridge cycling continues as long as intracellular [Ca2+] high enough to bind troponin C
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| muscle relaxation | occurs when [Ca2+] ↓ to resting levels
1)reaccumulated in sarcoplasmic reticulum=>Ca2+-ATPase
2)extruded from cell=>Ca2+ ATPase and Ca2+-Na+ exchange
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| inotropism | intrinsic ability of myocardial cells to develop force at given muscle cell length
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| positive inotropic effects | SNS=>beta1 receptors=>pathway phosphorylates sarcolemmal Ca2+ channels and phospholamban
1)↑ peak tension
2)↑ rate of tension development
3)faster rate of relaxation=>shorter contraction=>longer filling time
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| sarcolemmal Ca2+ channels | when phosphorylated
1)↑ inward Ca2+ current during plateau phase
2)↑ Ca2+ trigger=>↑ Ca2+ released from sarcoplasmic reticulum
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| phospholamban | protein that regulates Ca2+ ATPase in sarcoplasmic reticulum
when phosphorylated stimulates Ca2+ ATPase=>greater uptake and storage of Ca2+in sarcoplasmic reticulum leads to
1)faster relaxation
2)↑ amount of stored Ca2+ for future release
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| negative inotropic effects | PNS=>muscarinic receptors=>negative effect on ATRIA=>inhibitory pathway ↓ contractility
1)ACh ↓ inward Ca2+ current during plateau
2)ACh ↑ K+-Ach conduction=>shortens AP duration=>↓ inward Ca2+ current
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| heart rate and contractility | ↑ HR ↑ contractility and vice versa=>Ca2+ the underlying concept
1)greater influx of Ca2+ during AP=>greater accumulation of Ca2+=>↑ total amount of trigger Ca2+
2)↑ HR caused by SNS=>phospholamban phosphorylated
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| cardiac glycosides | positive inotropic agents=>inhibit Na+-K+ ATPase=>alters Ca2+-Na+ exchanger fxn=>[Na+] equilibrates [Ca2+] ↑=>↑ tension
derived from foxglove plan=>Digitalis purpurea=>used to treat CHF
ex) digoxin, digitoxin, ouabain
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| muscle length and Ca2+ (length-tension relationship) | increasing muscle length
1)↑ troponin C's Ca2+ sensitivity
2)↑ Ca2+ release from sarcoplasmic reticulum
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| preload | LVEDV=>resting length from which muscle contracts
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| afterload | aortic press=>velocity of shortening cardiac muscle maximal when afterload=0
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| stroke volume | vol of blood ejected by ventricle on each beat
SV=(EDV) - (ESV)
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| ejection fraction | fraction of EDV ejected in each SV=>meas of ventricular efficiency
EF=SV/EDV
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| Frank-Starling relationship/law of the heart | vol of blood ejected by ventricle depends on vol present in ventricle at end of diastole
EDV depends on venous return
law underlies and ensures CO=venous return
if VR ↑=>EDV ↑=>SV ↑
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| width of PV-loop | vol of blood ejected=SV
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| ventricular pressure loop phases | 1)isovolumetric contraction
2)ventricular ejection=>aortic valve opens; press reaches highest point
3)isovolumetric relaxation
4)ventricular filling=>mitral valve opens
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| PV loop-increased preload | ↑ VR=>↑ preload=>↑ SV
↑ SV based on Frank-Starling relationship
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| PV loop-afterload | ↑ aortic press=>SV ↓=>EDV ↑
*ventricular press must rise to greater-than-normal level during isovolumetric contraction
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| PV loop-increased contractility | ↑ contractility=>↑ tension and press=>↑ SV and EF
*EDV ↓
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| myocardial oxygen consumption | press work (internal work) more costly than vol work
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| aortic stenosis and myocardial O2 consumption | myocardial O2 consumption greatly ↑=>extra press work from ventricle to develop high press to pump blood thru stenosed aortic valve
*CO reduced
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| strenuous exercise and myocardial O2 consumption | myocardial O2 consumption ↑ from ↑ vol work
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| law of Laplace | greater wall thickness=>greater developed press
*explains ventricular wall hypertrophy=>but too much thickness can lead to ventricular failure
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| Fick principle | CO of left and right ventricles equal
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| cardiac cycle | 1)atrial systole
2)isovolumetric ventricular contraction
3)rapid ventricular ejection
4)reduced ventricular ejection
5)isovolumetric ventricular relaxation
6)rapid ventricular filling
7)reduced ventricular filling
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| cardiac cycle-atrial systole | preceded by P wave=>depol of atria=>artrial contraction=>↑ atrial press reflected in veins=>a wave
mitral valve open=>ventricles filling
*blip in ventricular press. during contraction=>active filling
S4 heard in ventricular hypertro
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| cardiac cycle-isovolumetric ventricular contraction | begins during QRS complex=>electrical activation of ventricles
mitral valve closes when L ventricular press>L atrial press;
tricuspid valve closes in R heart; *S1 heard=>splits bc mitral closes before tricuspid
press ↑ but vol constant
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| cariac cycle-rapid ventricular filling | ventricular press reaches highest value=>aortic valve opens
*MOST SV ejected=>aortic press ↑
atrial filling begins for ejection in next cycle
ends with beginning of T wave (end of ventricular contraction)
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| cardiac cycle-reduced ventricular ejection | reduced ejection=>aortic valve still open without any ventricular contraction=>ventricular press falls
aortic press falls because blood running off into arterial tree
ventricles begin to repolarize=>beginning of T wave
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| cardiac cycle-isovolumetric ventricular relaxation | begins after ventricles fully repolarized=>end of T wave
left ventricular press ↓ dramatically=>aortic valve closes(dicrotic notch)=>S2=>splits bc inspiration delays pulmonic valve closure
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| cardiac cycle-dicrotic notch | point in aortic press curve where aortic valve closes
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| cardiac cycle-rapid ventricular filling | ventricular press falls to lowest level(remains low bc relaxed)=>mitral valve opens=>ventricles start to fill rapidly=>S3
S3 normal in children-not adults=>only heard when in CHF(vol overload), advanced mitral/tricuspid regurgitation
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| cardiac cycle-reduced ventricular filing | longest phase of cardiac cycle
end of this phase marks end of diastole
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| mean systemic pressure | mean circulatory press if heart stopped=>press same throughout vasculature and equal to mean systemic press=>no blood flow=0 venous return
influences
1)blood vol
2)distribution of blood between stressed and unstressed vol
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| stressed volume | vol of blood that produces press by stretching elastic fibers in blood vessels=>vol in arteries
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| unstressed volume | vol of blood that produces no press=>blood in veins
when full ↑ blood vol moves into stressed vol
can hold
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| decrease in TPR and venous return | ↓ resistance ↑ venous return=>makes blood flow back to heart easier
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| increase in TPR and venous return | increases arterial press-->increases afterload-->decreases CO
increased resistance decreases venous return-->makes blood flow back to heart harder
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| mean arterial pressure | approx. 100 mmHg=>driving force for blood flow
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| baroreceptor reflex | fast and neurally mediated
1)BP sensors
2)afferent neurons=>carry info to brain
3)brain stem centers=>process info and coordinate response
4)efferent neurons=>direct changes in heart and blood vessels
keeps arterial press constant
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| baroreceptors | press sensors in
1)carotid sinus=>sensitive to ↑ and ↓ of arterial press
2)aortic arch=>sensitive to ↑ in arterial press
*more sensitive to rate of change in press
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| parasympathetic outflow effect on heart | vagus nerve ↓ heart rate via SA node
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| sympathetic outflow effect on heart | 1)↑ HR via SA node
2)effects cardiac muscle=>↑ contractility and SV
3)effects arterioles=>vasoconstriction and ↑ TPR
4)effects veins=>venoconstriction and ↓ of unstressed vol
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| hemorrhage and baroreceptor reflex response | hemorrhage ↓ arterial press=>↓ stressed vol
reflex tries to ↑ arterial presure
1)↓ PNS activity in heart
2)↑ SNS activity to heart and blood vessels =>↑ TPR and CO
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| valsalva maneuver | expiring against closed epiglottis (ex.coughing, defecation, heavy lifting)
↑ intrathoracic press=>↓ venous return=>↓ CO=>↓ arterial press
*HR should ↑ if baroreceptor reflex intact
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| RAA system | hormonally regulates blood vol=>arterial press
mechanoreceptors in afferent arterioles sense ↓ in renal perfusion press
in kidneys prorenin=>renin acts on angiotensinogen=>ATI(via ACE)=>ATII stimulates secretion of aldosterone and A
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| angiotensin II | acts on adrenal cortex=>stimulates synthesis and secretion of aldosterone
causes arteriolar vasoconstriction=>↑ TPR
acts on hypothalamus=>↑ thirst and secretion of ADH
stimulates Na+-H+ exchange in renal proximal tubule
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| aldosterone | secreted by zona glomerulosa cells of adrenal cortex
acts on principal cells of renal distal tubule and collecting ducts-->increase Na+ reabsorption-->increase ECF volume and blood volume
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| ADH | secreted by posterior pituitary=>secretion stimulates
1)increasing serum osmolarity
2)↓ in BP
V1 receptors in vascular smooth muscle=>vasoconstriction
V2 receptors in principal cells of renal collecting ducts=>↑ water reabsorptio
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| O2 peripheral chemoreceptors | located in carotid bodies and aortic bodies
1)sensitive to ↓ in Po2=>arteriolar vasoconstriction
2)sensitive to increasing Pco2 and ↓ pH
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| central chemoreceptors | located in medulla=>sensitive to changes in Pco2 and pH
brain intolerant of ↓ in blood flow
↑ sympathetic outflow=>intense arteriolar vasoconstriction and ↑ in TPR=>blood redirected to brain
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| Cushings reaction | ↑ ICP ↓ perfusion to brain=>stim central chemoreceptors=>↑ sympathetic outflow to blood vessels
1)↑ TPR
2)dramatically ↑ arterial press(can be life-threatening levels)
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| cardiopulmonary (low-pressure) baroreceptors | located in veins, atria, pulmonary arteries=>sense high blood vol
1)↑ secretion of ANP
2)secretion of ADH inhibited
3)renal vasodilation
4)↑ HR=>↑ CO=>↑ renal perfusion=>↑ Na+ and water excretion
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| atrial natriuretic peptide (ANP) | secreted by atria in response to ↑ atrial press
1)vasodilation and ↓ TPR
2)↑ Na+ and water excretion in kidneys=>↓ total body Na+ content, ECF vol, and blood vol
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| Starling equation | Jv=Kf[(Pc-Pi)-(πc-πi)]
(+) filtration
(-) absorption
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| Starling pressures | 1)capillary hydrostatic press=>favors filtration=>declines along length of capillary
2)interstitial hydrostatic press=>opposes filtration
3)capillary oncotic press [protein]=>opposes filtration
4)interstitial oncotic press=>favors filtration
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| lymphatic capillaries | lie in interstitial fluid close to vascular capillaries
have one-way valves=>interstitial fluid and protein enter only=>drain in thoracic duct=>empties in large veins
smooth muscle walls and muscle compression =>aids in flow back to thoracic du
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| edema | ↑ in interstitial vol that exceeds ability of lymphatics to return it to circulation
result of
1)lymph nodes surgically removed or irradiated
2)filariasis
3)parasitic infection of lymph nodes
4)lack of muscular activity
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| local control of blood flow | primary mechanism utilized to match blood flow with metabolic needs of tissue
exerted thru direct action of local metabolites on arteriolar resistance
1)autoregulation
2)active hyperemia
3)reactive hyperemia
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| neural or hormal control of blood flow | 1)SNS on vascular smooth muscle
2)vasoactive substances-histamine, bradykinin, prostaglandins
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| autoregulation of local blood flow | maintenance of constant blood flow to organ despite changing arterial press
1)achieved by immediate compensatory vasodilation of coronary arterioles
2)↓ resistance of coronary vasculature
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| active hyperemia | blood flow ↑ proportionately to meet ↑ metabolic demand
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| reactive hyperemia | blood flow ↑ in response to or reacting to a prior period of ↓ blood flow
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| myogenic hypothesis | explains autoregulation
1)when arterial press ↑=>arterioles stretch then contract=>maintains constant flow in face of ↑ press
2)when arterial press ↓=>arterioles relax and resistance ↓=>maintains constant flow
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| metabolic hypothesis | explains all local control of blood flow
basic premise: O2 delivery to tissue matches O2 consumption=>metabolic activity produces vasodilator metabolites (CO2, H+, K+, lactate, adenosine)
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| histamine | released in response to trauma=>powerful vascular effects
1)dilates arterioles
2)constricts venules
*large ↑ in capillary hydrostatic press=>↑ filtration=>edema
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| bradykinin | 1)dilation of arterioles
2)constriction of venules
*large ↑ in capillary hydrostatic press=>↑ filtration=>edema
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| serotonin | released in response to blood vessel damage=>local vasoconstriction=>reduce blood flow and blood loss
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| prostaglandins | various effects
1)prostacyclin and prostaglandin-E series=>vasodilators
2)thromboxane A2 and prostaglandin-F series=>vasoconstrictors
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| coronary circulation local blood flow control | almost entirely controlled by local metabolites
*most important local metabolic factors
1)hypoxia
2)adeosine
mechanical compression of blood vessels causes brief periods of occlusion during systole in cardiac cycle=>reactive hyperemia
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| cerebral circulation local blood flow control | almost entirely controlled by local metabolites
exhibits autoregulation, active and reactive hyperemia
*CO2 the most important local vasodilator
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| pulmonary circulation local blood flow control | controlled by O2=>hypoxia causes vasoconstriction=>shunts blood away from poorly ventilated areas where blood flow would be "wasted" and toward well-ventilated areas where gas exchange can occur
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| renal circulation local blood flow control | tightly autoregulated=>flow constant even when renal perfusion changes
result of myogenic properties of arterioles and tubuloglomerular feedback
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| skeletal muscle circulation local blood flow control | 1)at rest-sympathetic innervation; alpha1-vasoconstriction; beta2-vasodilation (predominates)
2)during exercise-local metabolites (ex. lactate, adenosine, K+); autoregulation, active and hyperactive hyperemia exhibited
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| skin circulation local blood flow control | contains dense sympathetic innervation=>alters blood flow to skin to regulate body temperature
vasoactive substances have effects (ex. histamine)
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| thyroid hormones | thermogenic hormones
1)stimulate Na+-K+ ATPase
2)↑ O2 consumption
3)↑ metabolic rate
4)↑ heat production
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| SNS generating heat mechanism | activated by cold temp and stim
1)brown fat=>↑ metabolic rate and heat production
2)alpha1 receptors=>vasoconstriction to reduce blood flow to surface of skin=>reduces heat loss
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| mechanism for dissipating heat | coordinated in anterior hypothalamus
1)↓ sympathetic activity in skin blood vessels=>heat loss
2)↑ activity of sweat glands
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| fever | abnormal elevation of body temp
produced by pyrogens=>↑ hypothalamic set-point temp
pyrogens ↑ prod of IL-1=>↑ PG prod=>↑ set-point temp
reduced by aspirin
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| aspirin and fever | reduces fever=>inhibits cyclooxygenase enzyme necessary to synthesize prostaglandins=>disrupts raise of set-point temperature
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| heat exhaustion | consequence of body's response to elevated environmental temperatures
excessive sweating can result in ↓ ECF vol, ↓ blood vol, ↓ arterial press, and fainting
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| heat stroke | body temperature ↑ to point of tissue damage
heat not properly dissipated=>core temperature ↑ to dangerous levels
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| malignant hyperthermia | massive ↑ in metabolic rate, ↑ O2 consumption, ↑ heat prod in skeletal muscle=>head dissipating mechanisms can't keep up
can be fatal if untreated
can be caused by inhalation anesthetics
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| orthostatic hypotension | occurs when someone stands up too quickly=>↓ in arterial blood press upon standing=>blood pools in the veins of lower extremities=>venous return and CO ↓=>↓ in mean arterial press
can cause light-headedness, fainting, edema
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| first degree heart block | slowing in AV conduction=>prolonged PR interval
each P wave does succeed in conducting through the AV conducting system to activate the ventricle
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| second degree heart block | only some P waves conduct through the AV junction=>ventricles don't get excited=>heart skips a beat
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| third degree heart block | complete block=>no P waves go thru AV conduction system to depolarize the ventricle
if block at AV node a focus lower in the AV junction becomes pacemaker=>rate is usually less than a normal sinus rate.
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|
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