Circulatory System (Heart) Flashcards
(120 cards)
1
Q
cardiovascular system
A
heart & blood vessels
2
Q
circulatory system
A
heart, blood vessels, AND the blood
3
Q
pulmonary circuit
A
-RIGHT SIDE of heart
-carries blood to LUNGS for gas exchange and back to heart
4
Q
systematic circuit
A
-LEFT SIDE of heart
-supplies oxygenated blood to all tissues of the body & returns to heart
5
Q
position of heart
A
located in mediastinum between lungs
6
Q
size & shape of heart
A
-base: wide, superior portion of heart, large vessels attach here
-apex: tapered inferior end, tilts to left
7
Q
pericardium
A
double-walled sac that encloses heart
8
Q
visceral perdicardium (epicardium)
A
serous membrane directly covering the heart
9
Q
parietal pericardium
A
superficial fibrous layer of connective tissue
10
Q
pericardial cavity
A
space inside the pericardial sac filled with pericardial fluid
11
Q
heart wall consists of:
the 3 layers?
A
epicardium, myocardium, endocardium
12
Q
epicardium (visceral pericadium)
A
-serous membrane covering the heart
-adipose in thick layer in some places
-coronary blood vessels travel through this layer
13
Q
endocardium
A
-smooth inner lining of heart & blood vessels
-covers valve surfaces and is continuous with endothelium of blood vessels
14
Q
myocardium
A
layer of cardiac muscles
* muscle spirals
15
Q
fibrous skeleton
A
framework of collagenous and elastic fibers
* provides structural support and
attachment for cardiac muscle
and anchor for valve tissue
* electrical insulation
16
Q
how many chambers are there?
A
4
17
Q
what are the superior chambers?
A
right and left atria, receive blood returning to heart
18
Q
what are the inferior chambers?
A
right and left ventricles, pump blood out of heart
19
Q
interatrial septum
A
outside of atria
20
Q
pectinate muscles
A
inner atria walls
21
Q
interventricular septum
A
between ventricles
22
Q
trabeculae carnae
A
may prevent ventricle walls from sticking together after contraction
23
Q
what do valves ensure?
A
they ensure one-way flow of blood through heart
24
Q
atrioventricular (AV) valves
A
control blood flow between atria and ventricles
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semilunar valves
control flow into great arteries
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the right AV valve is also called...
three cusps = tricuspid valve
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the left AV valve is also called...
two cusps = mitral valve
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chordae tendinae
connect AV valves to papillary muscles on floor of ventricles
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semilunar valves
control flow into great arteries; open and close because of blood flow & pressure
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pulmonary semilunar valve
opening between right ventricle & pulmonary trunk
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aortic semilunar valve
opening between left ventrile & aorta
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when ventricles relax...
-pressure drops in ventricles
-semilunar valves close
-AV valves open
-blood flows from atria to ventricles
33
when ventricles contract
-pressure rises in ventricles
-semilunar valves open
-AV valves close
-blood flows from ventricles to great vessels
34
how does blood flow through chambers?
1. blood enters right atrium from SVC & IVC
2. blood then goes through RIGHT AV valve (tricuspid valve)
3. blood goes through right ventricular
-contraction of right ventricular causes pulmonary valve to open
4. blood flows through pulmonary valve & pulmonary trunk
5. gas exchange occurs in lungs, unloads CO2 and loads O2.
-lung alevolies
-lung capillaries
-lung venules
6. blood returns via pulmonary veins
7. blood goes to left atria
8. blood flows through left AV valve (bicuspid valve) & then to left ventricle
-contraction of left ventricle forces aortic valve to open
9. blood flows through aortic valve into aorta
10. blood in aorta is distributed systematically, unloads O2 & loads CO2
11. blood returns via SVC or IVC
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coronary circulation
5 percent of blood pumped by heart is pumped to the heart iself
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arterial supply (LAC)
L: left coronary artery, branches of ascending aorta
A: anterior interventricular branch ("widowmaker")
C: circumflex branch, passes around left side of heart in coronary sulcus. gives off left marginal branch & then ends in posterior side of the heart.
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myocardial infarction
heart attck!!
-interruption of blood supply to the heart from a blood
clot or fatty deposit
-some protection from MI is provided by arterial anastomoses which provide alternative routes of blood flow
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arterial supply (RaMP)
R: right coronary artery, branches off ascending aorta, supplies sinoatrial node (pacemaker)
a
M: marginal branch (right)
P: posterior interventricular branch
38
when is flow through coronary arteries greatest?
when heart relaxes
-contraction compresses the coronary arteries & obstructs blood flow
-aortic valve flap opens during contraction covering the openings to coronary arteries
-during ventricular diastole, blood in the aorta surges back toward
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myocardial infarction (MI)
a heart attack!
–interruption of blood supply to heart from blood clot or fatty deposit
–some protection from MI is provided by arterial anastomoses which provide alternative routes of blood flow
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angina pectoris
chest pain from partial
obstruction of coronary blood flow: pain caused by ischemia of cardiac muscle
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venous drainage
5% to 10% of coronary blood drains directly into heart chambers (mostly right ventricle) by way of the thebesian veins
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most coronary blood returns to right atrium by...?
coronary sinus.
–large transverse vein in
coronary sulcus on
posterior side of heart
–collects blood and
empties into right atrium
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3 main inputs of coronary sinus
great cardiac vein
middle cardiac vein
left marginal vein
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cardiocytes
striated, short, thick, branched cells, one
central nucleus
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intercalated discs
joins cardiocytes end to end with three
features: interdigitating folds, mechanical junctions, and
electrical junctions
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interdigitating folds
increase surface area
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desmosomes
mechanical linkages, prevent cardiocytes from being pulled apart
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gap junctions
allow ions to flow b/w cell; can stimulate neighbors
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what does the metabolism of cardiac muscle depend on?
-depends on aerobic respiration to make ATP therefore requires huge mitochondria
-adaptable to different organic fuels =
fatty acids (60%); glucose (35%); ketones, lactic acid,
and amino acids (5%)
-more vulnerable to oxygen deficiency than lack of a
specific fuel
-fatigue resistant because it makes little use of anaerobic fermentation or oxygen debt mechanisms, Does not fatigue for a lifetime
50
the conduction system does what...?
coordinates the heartbeat
autorhythmic: has its own pacemaker & electrical system
-composed of an internal pacemaker & nerve-like conduction pathways through myocardium
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what is the SA node/pacemaker made up of and what does it do?
-sinoatrial (AV) node: modified cardiocytes
-pacemaker initiates each heartbeat and determines HR
*pacemaker is in right atrium near base of superior vena cavae
-signals spread throughout atria
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the conduction system consists of:
-atrioventricular (AV) node
-atrioventricular (AV) node bundle (bundle of His) & branches
-purkinje fibers
*cardiocytes then pass signal cell to cell through gap junctions
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the conduction system summarized
1. sa node fires
2. excitation spreads through atrial myocardium
3. av node fires
4. excitation spreads down AV bundle
5. purkinje fibers distribute excitation through ventricular myocardium
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sympathetic nerves
increase HR and contraction strength
*cardioacceleratory
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parasympathetic nerves
slow HR
*cardioinhibitory
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systole
contraction
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diastole
relaxation
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sinus rhythm
normal heartbeat triggered by SA node regularly 60-100 bpm (adult at rest 70-80 bpm)
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ectopic focus
a region of spontaneous firing other than SA node
-may govern heart rhythm if SA node is damaged
nodal rhythm: if SA node is damaged HR is set to AV node (40 to 50bpm)
*other ectopic focal rhythms are 20-40 bpm & too slow to sustain life
60
pacemaker physiology
1. starts at -60mV and drifts upward due to slow NA inflow, SA node does not have a stable RMP
*gradual depolarization is called pacemaker potential
2. when it reaches threshold of -40 mV, fast voltage-gated CA channels to open & closing Na inflow
*faster depolarization occurs peaking at 0mV
3. Ca channels close and K channels then open allowing K to leave the cell
*causing repolarization
*once K channels, pacemaker potential starts over
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3 phases of cardiocyte action potential
1. depolarization
2. plateu
3. repolarization
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electrical behavior of the myocardium
(step by step)
1. depolarization phase (very brief) -90 RMP
*stimulus opens volatge-regulated Na gates (Na rushes in), membrane depolarizes rapidly
2. starts at +30 RMP, plateu phase sustains contraction for expulsion of blood from heart, as Ca opened it flows in & K also opens it flows out PLATEU
*voltage gated slow Ca channels (Ca comes in)
3. repolarization phase
*Ca channels close, K open, rapid diffusion of K occurs, returning cell to RMP
63
electrical behavior of the myocardium summarized
1. Na gates open
2. rapid depolarization occurs
3. Na gates close
4. slow CA channels open, some K leakage causing plateu
5. Ca channles then close, K channels open with rapid diffusion causing repolarization
64
electrocardiogram (ECG or EKG)
composite of all action potentials of nodal and myocardial cells detected, amplified, and recorded by electrodes on arms, leg, and chest
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the electrocardiogram summarized
| step by step
1. atrial depolarization begins:
2. atrial depolarization complete (atria now contracted):
3. ventricles begin to depolarize at apex; atria repolarized (atria relaxed):
4. ventricular depolarization complete (ventricles now contracted):
5. ventricles begin to repolarize at apex
6. ventricular repolarization complete (ventricles relaxed)
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P wave
SA node fires, atria depolarize & contract
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QRS complex
ventricular depolarization
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ST segment
ventricular systole
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T wave
ventricular repolarization and relaxation (end of diastole)
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what issues can an ECG show us?
-MI
-abnormalities in conduction pathway
-heart enlargement
-electrolyte & hormone imbalance
66
ventricular fibrillation
serious arrhythmia caused by electrical signals
traveling randomly
*heart cannot pump blood; no coronary perfusion
-hallmark of heart attack (MI)
*kills quickly if not stopped
defibrillation—strong electrical shock with intent to depolarize entire myocardium and reset heart to sinus rhythm, may allow time for other corrective action
67
heart block
failure of conduction system to conduct
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premature ventricular contraction
extra beats due to ventricular ectopic focus
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cardiac cycle
one complete contraction and relaxation of all 4 chambers
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2 main variables govern fluid movement
1. pressure CAUSES flow
while
2. resistant OPPOSES flow
-fluid will only flow is there is a pressure gradient (high to low)
*pressure measured in mm Hg with a manometer
71
mitral valve prolapse
insufficiency in which one or both mitral valve cusps bulge into atria during ventricular contraction
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valvular insufficiency (incompetence)
any failure of a valve to prevent reflux, the backward flow of blood
(type of heart murmur)
73
valvular stenosis
cusps are stiffened and opening is constricted by scar tissue
-resulted of rheumatic fever, autoimmune attack on mitral & aortic valves
74
heart murmur
abnormal heart sound produced by regurgitation of blood through incompetent valves
75
what are the heart sounds?
auscultation
S1: louder and longer "lub," occurs with closure of AV valves
S2: softer and sharper "dup," occurs with closure of semilunar valves
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valvular insufficiency
| heart murmur
cardiac valves leaking because cusps not closing tightly
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valvular stenosis
valve cusps scarred and cannot open completely
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5 phases of the cardiac cycle
1. atrial contraction & ventricular filling
2. isovolumetric contraction
3. ventricular ejection
4. isovolumetric relaxation
5. atrial relaxation & ventricular filling
entire cardiac cycle is completed in ~0.8s
79
atrial contraction and ventricular filling
-AV valves open (p wave)
-atrial systole initiated by the SA node
-this moves remainder of blood from each atrium into ventricles
-ventricles now hold their maximum
end diastolic volume (EDV) of 130 mL
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isovolumetric contraction
| stage 2
QRS complex
-ventricular systole and closing of AV valves
-SL valves remain closed
-"isovolumetric" with all valves closed
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ventricular ejection
-ventricular systole continues and SL valves open
-blood is ejected from the ventricles
*stroke volume = 70 mL
*end-systolic volume (ESV) 130 mL - 70mL = 60 mL
T wave begins
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isovolumetric relaxation
-ventricular diastole begins
-SL valves close
-AV valves have not yet opened
-"isovolumetric"
T wave ends
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atrial relaxation & ventricular filling
-rising pressures in the atria cause AV valves to open
p wave
-begin the cycle again
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overview of vol. changes
end-systolic volume (ESV): 60 mL
passively added to ventricle during atrial diastole: +30 mL
added by atrial systole: +40 mL
total -> end-diastolic volume (EDV): 130 mL
stroke volume (SV) ejected by ventricular systole: -70 mL
leaves: end-systolic volume (ESV): 60 mL
85
overview of volume changes (right ventricular)
1. right ventricular output exceeds left ventricular output
2. pressure backs up
3. fluid accumulates in pulmonary tissue
-if the left ventricle pumps less blood than the right, the blood pressure backs up into the
lungs and causes pulmonary edema
86
overview of volume changes (left ventricular)
1. left ventricular output exceeds right ventricular output
2. pressure backs up
3. fluid accumulates in systematic tissue
If the right ventricle pumps less blood than the left, pressure
backs up in the systemic circulation
and causes systemic edema
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what is cardiac output?
CO: amount of blood ejected by each ventricles in 1 min
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cardiac output equation
CO = HR x SV
abt 4 to 6 L/min at rest
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cardiac reserve
the difference between person's maximum and resting CO
-increases with fitness, decreases with disease
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pulse
surge of pressure produced by heart beat that can be felt by palpating a superificial artery
-infants have HR of 120 bpm or more
-females: 72-80 bpm, males: 64-72 bpm
-HR raises in elevates in elderly
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tachycardia
HR above 100
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bradycardia
less than 60
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positive chronotropic agents
factors that RAISE the HR (sympathetic)
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negative chronotropic agents
factors that lower the HR (parasympathetic)
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chronotropic effects of the ANS
-ANS does not initiate the heart beat, it modulates rhythm
-cardiac centers initiate autonomic output to the heart
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cardiostimulatory effect
some neurons of the cardiac center transmit signals to the heart by way of sympathetic pathways
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cardioinhibitory effect
others transmit parasympathetic signals by way of the vagus nerve
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sympathetic postganglionic fibers are
adrenergic!!
-releases norepinephrine
-lead to opening of Ca channels in plasma membrane
-increased Ca inflow accelerates depolarization of SA node
-by accelerating both, contraction & relaxation, norepinephrine increases HR as high as 230 bpm
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parasympathetic vagus nerves have
cholinergic; inhibitory effects on SA and AV nodes
-acetylcholine (ACh) binds to muscarinic receptors
-opens K gates in nodal cells
-as K leaves the cells, they become hyperpolarized and fire less frequently
-heart slows down
100
vagal tone
holds down the HR to 70-80 bpm at rest
-steady background firing rate of the vagus nerve
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w/out influence from cardiac centers...
the heart has an intrinsic firing rate at 100 bpm
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baroreceptors
signal cardiac center (an input to cardiac center)
-pressure sensors in aorta & internal carotid arteries
-if BP decreases, signal rate drops, cardiac center increases HR
-if BP increases, signal rate rises, cardiac center decreases HR
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chemoreceptors
signals cardiac center, as well.
-in aortic arch, carotid arteries, and medulla oblongata
-sensitive to blood pH, CO2, and O2 levels
-more important in respiratory control than cardiac control
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baroreflexes and chemoreflexes are both what type of feed back loops?
negative
-responses to fluctuation in BP & chemistry
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what chemicals affect HR?
-neurotransmitters: NE & Ach
-adrenal catecholamines: NE & epinephrine
*nicotine stimulates
*TH increases
*caffein prolongs adrenergic effect
*cocaine inhibits norepinephrine
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electrolytes
K (has greatest chronotropic effect)
-hyperkalemia: excess K diffuses
into cardiocytes
-hypokalemia: deficiency in K
calcium
-hypercalcemia: excess of Ca2+
-hypocalcemia: deficiency of C
107
stroke volume and its 3 variables govern SV
volume of blood pumped by one ventricle per pump
1. preload
2. contractility
3. afterload
108
preload
amount of tension in ventricular myocardium immediately before it begins to contract
-increased preload causes increased force of
contraction
–exercise increases venous return and stretches
myocardium
-cardiocytes generate more tension during
contraction
–increased cardiac output matches increased
venous return
109
Frank-Starling law of the heart
SV & EDV are proportional
-stroke volume is proportional to the end diastolic
volume
-ventricles eject almost as much blood as they
receive
-the more they are stretched, the harder they
contract
110
contractility
refers to how hard myocardium contracts for a given preload
111
positive inotropic agents...
increase contractility
-hypercalcemia can cause strong, prolonged contractions
-catecholamines increase calcium levels
-glucagon stimulates cAMP production
112
negative inotropic agents
reduce contractility
-hypocalcemia can cause weak, irregular heartbeat and cardiac arrest in diastole
–hyperkalemia reduces strength of myocardial action potentials and the release of Ca2+ into the
sarcoplasm
113
afterload
sum of all forces opposing ejection of blood from ventricle
-largest part of after load is BP in aorta & pulmonary trunk
* opposes the opening of SL valves
* limits SV
-hypertension increases afterload & opposes ventricular ejection
-anything that impedes arterial circulation can also increase after load
114
variables that influence after load
artheroclerosis, which is deposition of plaque on inner lining of arteries, is typically only a factor as we age
-arteries become more narrow in diameter
-increases the resistance to pump blood into the arteries
-stroke volume decreases
