Cardiovascular System Flashcards
(134 cards)
1
Q
right side of the heart
A
lungs
receives unoxygenated blood
lungs get rid of the CO2
thinner and flatter
crescent shape
2
Q
left side of the heart
A
systemic-lungs to body
carries oxygenated blood from the lungs through the system
thicker walls
round
3
Q
pulmonary arteries
A
pump blood out
4
Q
pulmonary veins
A
pump blood in
5
Q
apex of the heart
A
bottom aspect of the heart
6
Q
Diaphragm is higher on the ___ side
A
right
7
Q
heart location
A
mediastenum of the chest between the 2nd and 5th intercostal space
8
Q
heart rate vs pulse
A
rate-listen
pulse-feel
9
Q
pericardium
A
ceran wrap aorund the heart
3 layers (endocardium, myocardium, and visceral epicardium)
10
Q
pericarditis
A
inflammation of pericardium
roughens membrane surface and causes pericardial friction rub (creaking) that can be heard with a stethescope (sounds like sandpaper or crackling)
11
Q
cardiac temponade
A
excess fluid that leaks into pericardial space
can compress the heart’s pumping ability
treatment-fluid drawn out with syringe
12
Q
epicardium
A
visceral layer of serous pericardium
parietal-outer
visceral-inner
13
Q
myocardium
A
circular or spiral bundles of contractile and noncontractile cardiac muscle cells
noncontractile tissues are the pacemaker cells that contract by themselves w/o outside help
14
Q
endocardium
A
innermost layer; continuous with endothelial lining of blood vessels
lines the heart chambers and covers the cardiac skeleton of valves
15
Q
role of heart valves
A
ensures unidirectional blood flow through the heart with no backflow
16
Q
what causes the valves to open/close
A
pressure changes
pressure builds-valves close
low pressure-valves open
17
Q
two major types of valvues
A
semilunar and atrioventricular
18
Q
SL valves
A
located between the ventricles and major arteries
pulmonary and aortic
19
Q
AV valves
A
located between the atria and ventricles
tricuspid-right
bicuspid-left
20
Q
incompetent valve (mitral regurgitation)
A
blood backflows so the heart repumps the same blood over and over again
21
Q
valvular stenosis (mitral stenosis)
A
stiff flaps that constrict the opening
heart needs to exert more force to pump blood
22
Q
blood flow through the right side of the heart
A
Superior vena cava (SVC), inferior vena cava (IVC), and coronary sinus →
Right atrium →
Tricuspid valve →
Right ventricle →
Pulmonary semilunar valve →
Pulmonary trunk →
Pulmonary arteries →
Lungs
23
Q
blood flow through the left side of the heart
A
Four pulmonary veins →
Left atrium →
Mitral valve →
Left ventricle →
Aortic semilunar valve →
Aorta →
Systemic circulation
24
Q
coronary arteries
A
functional blood supply to the heart itself
shortest circulation in the body
during relaxation, coronary arteries profuse the heart (diastole)
myocardium of the left ventricle receives the most blood
start from the aorta
25
left coronary artery
supplies interventricular septum, anterior ventricular walls, left atrium, and posterior wall of left ventricle
2 branches: anterior interventricular artery and circumflex artery
26
right coronary artery
supplies right atrium and most of right ventricle
two branches: right marginal artery and posterior interventricular artery
27
anterior interventricular artery (also called left anterior descending artery)
oxygenated blood to 70% of the heart
BIG PROBLEM WHEN BLOCKED
28
circumflex artery
29
posterior interventricular artery
heart ryhthms
30
right marginal artery
31
angina pectoris
Thoracic pain caused by fleeting deficiency in blood delivery to myocardium
cells are weakened
32
myocardial infarction (heart attack)
prolonged coronary blockage
areas of cell death are repaired with noncontractile scar tissue
blocked left anterior often leads to immediate death
33
compare and contrast cardiac and skeletal muscle
same:
- both are contractile tissues
- both types of muscle contraction are preceded by depolarization in the form of an action potential (AP)
- both require the sarcoplasmic reticulum (SR) to release Calcium (Ca2+)
different:
- some cardiac cells are self-excitable
- the heart contracts as a unit
- special Ca2 channels
- no tetanic contractions
- must have aerobic respiration (heart cannot function without oxygen)
34
contractile cells
responsible for contraction
35
pacemaker cells
noncontractile cells that spontaneously depolarize and initiate depolarization of the whole heart-automaticity
36
desmosomes
prevent adjacent cells from separating during contraction
37
gap junctions
allow ions to pass from cell to cell, transmitting current across the entire heart
38
special Ca2+ channels
influx of Ca2+ from extracellular fluid triggers Ca2+ release from SR
secondary calcium release channels triggered by og small influx of calcium
39
absolute refractory period
rest period almost as long as contraction
allows heart to refill again
40
depolarization
reaches threshold of 40 volts and calcium influx
41
repolarization
calcium channel inactive and potassium activated
42
cardiac action potentials
action potential is initiated bc of sodium opening and potassium closing.
sodium makes membrane more positive.
depolarization from sodium making it positive.
at threshold depolarization occurs and calcium comes in.
after this, potassium reopens, and sodium closes, and the membrane becomes more negative.
43
where are the pacemaker cells found?
SA node (sinus atrial node)
If SA isn't working, it goes to AV node.
If AV node isn't working, it goes to Bundle of His
If the Bundle of His isn't working, then to bundle branch and Purkinje fibers.
If AV and Sa aren't working, depends completely on ventricles.
44
sequence of excitation
Takes .22 seconds.
1. SA node depolarizes-sodium in, potassium stopped.
- SA node generates about 75 beats/min.
2. .1 second pause-ventricles refill
3. AV bundle
- The inherent heartbeat of AV node in absence of SA node is 50 beats/min.
4. Bundle branches
- Left and right are the 2 pathways down the interventricular septum to Purkinje fibers.
- Inherent heart rate will be 30 beats/min if AV doesn't work.
45
arrythmias
irregular heart rythms
uncoordinated artrial and ventricular contractions
46
fibrillation
rapid, irregular contractions
heart becomes useless for pumping blood, causing circulation to cease; may result in brain death
treatment: defibrillation interrupts chaotic twitching, giving the heart “clean slate” to start regular, normal depolarizations
47
ectopic foci
caused by defective SA node
48
defective AV node
heart block
treatment: pacemaker
49
cardioacceleratory center
sympathetic
stimulates SA and AV nodes, heart muscle, and coronary arteries
50
cardioinhibitory center
parasympathetic
inhibits SA and AV nodes via vagus nerves
51
P wave
depolarization of SA node and atria
no pwave=no artial depolarization
52
QRS complex
ventricular depolarization and atrial repolarization
53
T wave
ventricular repolarization
54
PR interval
beginning of atrial excitation to beginning of ventricular excitation
55
ST segment
entire ventricular myocardium depolarized
prolonged/shortened=ventricles taking dif amounts of time to repolarize
56
QT interval
beginning of ventricular depolarization through ventricular repolarization
57
systole
period of heart contraction
58
diastole
period of heart relaxation
59
cardiac cycle
blood flow through the heart during one complete heartbeat
atrial systole and diastole followed by ventricular systole an diastole
phases: ventricular filling, isovolumetric contraction, ventricular ejection, isovolumetric relaxation
about .8 seconds (atrial systole .1 sec, ventricular systole .3 sec, and quiescent period about .4 sec)
60
ventricular filling stage (mid to late diastole)
80% of blood flows passively from artria through open AV valves into the ventricles (SL valves closed)
atrial depolarization triggers atrial systole (p wave) and the atria contracts pushing the remaining 20% of the blood into the ventricles (EDV-blood left in ventricles at end of ventricular diastole)
depolarization spread to ventricles (QRS complex)
atria finishing contracting and returns to diastole while the ventricle begin systole
AV valve opens, SL valves closed
SA node to AV node
61
isovolumetric contraction
atria relaxes and ventricles begin to contract
rising ventricular pressure causes closing of AV valves
split-second period when ventricles are completely closed (all valves closed), volume remains constant, ventricles continue to contract
ventricular pressure exceeds pressure in large arteries=SL valves are forced open
pressure in aorta reaches about 120 mm Hg
all blood in ventricles-pressure is greater in ventricles-AV valves close.
pressure isn’t high enough to release SL valves yet.
62
isovolumetric relaxation (early diastole)
following ventricular repolarization (T wave), ventricles relax
end systolic volume (ESV): volume of blood remaining in each ventricle after systole (should not be a lot left after, or heart is ineffective)
ventricular pressure drops causing backflow of blood from aorta and pulmonary trunk that triggers closing of SL valves
aorta and pulmonary have higher pressure-SL valves close.
ventricles are completely closed chambers momentarily
63
normal heart rate
about 75 beats/min
64
first heart sound (lub)
closing AV valves at beginning of ventricular systole.
65
second heart sound (dup)
closing of SL valves at beginning of ventricular diastole
66
pause between lub-dups
heart relaxation
67
aortic heartbeat
heard at 2nd intercostal space
68
mitral heart beat
heard at apex
69
tricuspid heart beat
heard at sternal margin of the 5th intercostal space
70
heart murmurs
abnormal heart sounds when blood hits obstructions
usually valve issues
71
cardiac output
amount of blood pumped out by each ventricle in 1 minute
heart rate x stroke volume
72
stroke volume
volume of blood pumped out by 1 ventricle with each beat (correlated to force of contraction)
SV=EDV-ESV (normal SV=120 ml-50ml=70 ml/beat
regulated by ANS, hormones, and ions
remain relatively constant
73
cardiac index
cardiac output x body surface area
3L/min/m2
74
what factors increase cardiac output?
increased stroke volume
faster heart beat
75
cardiac reserve
difference between resting and maximal CO
76
what are the main factors that affect stroke volume?
preload, contractility, and afterload
77
preload
degree of stretch of heart muscles just before they contract
most important factor is venous return
78
contractility
positive ionotropic: increase in contractility
- epinephrine and norepinephrine
- promotes calcium influx
- lowers ESV
negative ionotropic: decrease in contractility
- reduced sympathetic stimulation=reduced contractility
- acidosis, increased potassium, blocked calcium channels
79
afterload
back pressure exerted by arterial blood; the pressure the ventricles must overcome to eject blood
aortic pressure~80 mmHg
pulmonary trunk pressure~10 mmHg
increased by hypertension
increase=increased ESV=decreased SV
80
Frank Starling Mechanism
relationship between preload and SV
changes in preload cause changes in SV
81
chronotropic effect
any mechanism that alters cardiac rate
82
positive chronotropic effect
increases HR
83
negative chronotropic effect
decreases HR
84
HR can be regulated by...
ANS, chemicals (ions and hormones), age, gender, exercise, and body temp
85
ejection friction
best indicator of cardiac function
% of blood ejected from ventricles relative to the volume in the ventricles b4 contraction
normal=60%-70%
86
tachycardia
fast HR (over 100 beats/min)
87
bradycardia
slow HR (under 60 beats/min)
88
congestive heart failure (CHF)
inadequate circulation
weakened myocardium
persistent high BP is most common cause of heart failure
left-sided failure: pulmonary congestion (blood backs up in the lungs)
- SOB and wet cough
right-sided failure: peripheral congestion
- blood pools in body organs causing edema
failure of one side weakens the other
89
elastic arteries
thick-walled with large, low-resistance lumen
act as pressure reservoirs that expand and recoil as blood is ejected from the heart
aorta and its major branches
90
muscular arteries
deliver blood to body organs
active in vasoconstriction
91
arterioles
smallest arteries
control flow into capillary beds via vasodilation and vasoconstriction of smooth muscle
lead to capillary beds
92
capillaries
microscopic vessels; diameters so small only a single RBC can pass through at a time
supply almost every cell except for cartilage, epithelia, cornea, and lens of the eye
functions: exchange of gases, nutrients, wastes, hormones between blood and interstitial fluid
93
continuous capillaries
abundant in skin, muscles, lungs, and CNS
94
fenestrated capillaries
occurs in areas of active filtration (kidneys) or absorption (small intestine) and areas of endocrine hormone secretion
allow for increased permeability
95
sinusoidal capillaries
fewer tight junctions; usually fenestrated with larger intercellular clefts; incomplete basement membranes
occur in liver, bone marrow, spleen, and adrenal medulla
allow large molecules and even cells to pass across their walls
96
terminal arteriole
exchange of gases, nutrients, and wastes from surrounding tissue takes place in capillaries
97
capillary bed
an interwoven network of capillaries between the arterioles and venule
98
vascular shunt
channel that directly connects arteriole with venule (bypasses true capillaries)
99
precapillary sphincter
acts as valve regulating blood flow into the capillary bed
100
blood flow control
arteriole and terminal arteriole dilated when blood needed; constricted to shunt blood away from bed when not needed
101
veins
carry blood towards the heart
large lumen and thin walls make veins good storage vessels
contains up to 65% of blood supply
102
venous valves
prevent backflow of blood
most abundant in veins in limbs
103
venous sinuses
flattened veins with extremely thin walls
104
varicose veins
dilated and painful veins due to incompetent (leaky) valves
105
blood volume
volume of blood flowing through a vessel, organ, or entire circulation in a given period
overall is relatively constant when at rest, but at any given moment, varies at individual organ level, based on needs
106
blood pressure
force per unit area exerted on the wall of blood vessels by blood
107
total blood vessel length
longer=more resistance
108
greatest influence on resistance
blood vessel diameter
109
relationship between flow, pressure, and resistance
pressure increases=blood flow speeds up
resistance increases=blood flwo decreases
110
steepest drop in BP occurs where?
arterioles
111
mean arterial pressure (MAP)
pressure that propels blood to tissues
diastolic pressure + 1/3 pulse pressure (normal=93 mmHg)
112
muscular pump
contraction of skeletal muscles “milks” blood back toward the heart; valves prevent backflow
113
respiratory pump
pressure changes during breathing move blood toward the heart by squeezing abdominal veins as thoracic veins expand
114
sympathetic vasoconstriction
under sympathetic control, smooth muscles constrict, pushing blood back toward heart
115
capillary BP
ranges from 35 mm Hg at the beginning of the capillary bed to ∼17 mm Hg at the end of the bed
116
venous BP
small pressure gradient; about 15 mmHg
117
3 main factors regulating BP
cardiac output, peripheral resistance, blood volume
118
short term regulation of BP
neural controls (baroreceptors and chemoreceptors) and hormonal controls
119
neural controls
maintain MAP by altering blood vessel diameter and altering blood distribution in response to various organ demands
alter blood vessel diameter which alters resistanceor alter blood distribution to organs in response to specific demands
baroreceptors and chemoreceptors
120
baroreceptors
pressure sensitive mechanoreceptors that respond to changes in arterial pressure and stretch
vasodilation
decreased CO
121
chemoreceptors
detect increase in CO2, or drop in pH or O2
cause increased BP by increasing CO or increasing vasoconstriction
122
hormonal controls
adrenal medulla hormones (epinephrine and norepinephrine), angiotensin 2, ADH, and atrial natriuretic peptide
123
long term regulation of BP
renal controls alter blood volume via kidneys by direct renal mechanism or indirect renal mechanism
124
direct renal mechanism
alters blood volume independently of hormones
increased BP/blood volume=increased urine output to decrease BP
decreased BP/blood volume=kidneys conserve water and BP rises
125
indirect renal mechanism (renin-angiotensin-aldosterone)
decreased arterial BP=release renin from kidneys
angiotension to angiotension 1
ACE from the lungs converts angiotensin 1 to angiotensin 2
stimulates aldosterone secretion which causes ADH to be released
triggers thirst center-drink more water
acts as potent vasoconstrictor-increased BP
126
primary hypertension
90% of cases
no underlying cause identified
no cure but can be controlled
127
secondary hypertension
less common
due to identifiable disorders
treatment focuses on underlying disorder
128
orthostatic hypotension
temporary low BP and dizziness when suddenly rising from sitting or reclining position
129
chronic hypotension
a hint of poor nutrition and warning sign for Addison’s disease or hypothyroidism
130
acute hypotension
an important sign of circulatory shock
131
circulatory shock
Condition where blood vessels inadequately fill and cannot circulate blood normally
132
hypovolemic shock
from large scale blood loss
133
vascular shock
from extreme vasodilation and decreased peripheral resistance
134
cardiogenic shock
when an inefficient heart cannot sustain adequate circulation.
