Cardiovascular System Flashcards
right side of the heart
lungs
receives unoxygenated blood
lungs get rid of the CO2
thinner and flatter
crescent shape
left side of the heart
systemic-lungs to body
carries oxygenated blood from the lungs through the system
thicker walls
round
pulmonary arteries
pump blood out
pulmonary veins
pump blood in
apex of the heart
bottom aspect of the heart
Diaphragm is higher on the ___ side
right
heart location
mediastenum of the chest between the 2nd and 5th intercostal space
heart rate vs pulse
rate-listen
pulse-feel
pericardium
ceran wrap aorund the heart
3 layers (endocardium, myocardium, and visceral epicardium)
pericarditis
inflammation of pericardium
roughens membrane surface and causes pericardial friction rub (creaking) that can be heard with a stethescope (sounds like sandpaper or crackling)
cardiac temponade
excess fluid that leaks into pericardial space
can compress the heart’s pumping ability
treatment-fluid drawn out with syringe
epicardium
visceral layer of serous pericardium
parietal-outer
visceral-inner
myocardium
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
endocardium
innermost layer; continuous with endothelial lining of blood vessels
lines the heart chambers and covers the cardiac skeleton of valves
role of heart valves
ensures unidirectional blood flow through the heart with no backflow
what causes the valves to open/close
pressure changes
pressure builds-valves close
low pressure-valves open
two major types of valvues
semilunar and atrioventricular
SL valves
located between the ventricles and major arteries
pulmonary and aortic
AV valves
located between the atria and ventricles
tricuspid-right
bicuspid-left
incompetent valve (mitral regurgitation)
blood backflows so the heart repumps the same blood over and over again
valvular stenosis (mitral stenosis)
stiff flaps that constrict the opening
heart needs to exert more force to pump blood
blood flow through the right side of the heart
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
blood flow through the left side of the heart
Four pulmonary veins →
Left atrium →
Mitral valve →
Left ventricle →
Aortic semilunar valve →
Aorta →
Systemic circulation
coronary arteries
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
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
right coronary artery
supplies right atrium and most of right ventricle
two branches: right marginal artery and posterior interventricular artery
anterior interventricular artery (also called left anterior descending artery)
oxygenated blood to 70% of the heart
BIG PROBLEM WHEN BLOCKED
circumflex artery
posterior interventricular artery
heart ryhthms
right marginal artery
angina pectoris
Thoracic pain caused by fleeting deficiency in blood delivery to myocardium
cells are weakened
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
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)
contractile cells
responsible for contraction
pacemaker cells
noncontractile cells that spontaneously depolarize and initiate depolarization of the whole heart-automaticity
desmosomes
prevent adjacent cells from separating during contraction
gap junctions
allow ions to pass from cell to cell, transmitting current across the entire heart
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
absolute refractory period
rest period almost as long as contraction
allows heart to refill again
depolarization
reaches threshold of 40 volts and calcium influx
repolarization
calcium channel inactive and potassium activated
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.
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.
sequence of excitation
Takes .22 seconds.
- SA node depolarizes-sodium in, potassium stopped.
- SA node generates about 75 beats/min. - .1 second pause-ventricles refill
- AV bundle
- The inherent heartbeat of AV node in absence of SA node is 50 beats/min. - 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.
arrythmias
irregular heart rythms
uncoordinated artrial and ventricular contractions
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
ectopic foci
caused by defective SA node
defective AV node
heart block
treatment: pacemaker
cardioacceleratory center
sympathetic
stimulates SA and AV nodes, heart muscle, and coronary arteries
cardioinhibitory center
parasympathetic
inhibits SA and AV nodes via vagus nerves
P wave
depolarization of SA node and atria
no pwave=no artial depolarization
QRS complex
ventricular depolarization and atrial repolarization
T wave
ventricular repolarization
PR interval
beginning of atrial excitation to beginning of ventricular excitation
ST segment
entire ventricular myocardium depolarized
prolonged/shortened=ventricles taking dif amounts of time to repolarize
QT interval
beginning of ventricular depolarization through ventricular repolarization
systole
period of heart contraction
diastole
period of heart relaxation
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)
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
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.
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
normal heart rate
about 75 beats/min
first heart sound (lub)
closing AV valves at beginning of ventricular systole.
second heart sound (dup)
closing of SL valves at beginning of ventricular diastole
pause between lub-dups
heart relaxation
aortic heartbeat
heard at 2nd intercostal space
mitral heart beat
heard at apex
tricuspid heart beat
heard at sternal margin of the 5th intercostal space
heart murmurs
abnormal heart sounds when blood hits obstructions
usually valve issues
cardiac output
amount of blood pumped out by each ventricle in 1 minute
heart rate x stroke volume
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
cardiac index
cardiac output x body surface area
3L/min/m2
what factors increase cardiac output?
increased stroke volume
faster heart beat
cardiac reserve
difference between resting and maximal CO
what are the main factors that affect stroke volume?
preload, contractility, and afterload
preload
degree of stretch of heart muscles just before they contract
most important factor is venous return
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
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
Frank Starling Mechanism
relationship between preload and SV
changes in preload cause changes in SV
chronotropic effect
any mechanism that alters cardiac rate
positive chronotropic effect
increases HR
negative chronotropic effect
decreases HR
HR can be regulated by…
ANS, chemicals (ions and hormones), age, gender, exercise, and body temp
ejection friction
best indicator of cardiac function
% of blood ejected from ventricles relative to the volume in the ventricles b4 contraction
normal=60%-70%
tachycardia
fast HR (over 100 beats/min)
bradycardia
slow HR (under 60 beats/min)
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
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
muscular arteries
deliver blood to body organs
active in vasoconstriction
arterioles
smallest arteries
control flow into capillary beds via vasodilation and vasoconstriction of smooth muscle
lead to capillary beds
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
continuous capillaries
abundant in skin, muscles, lungs, and CNS
fenestrated capillaries
occurs in areas of active filtration (kidneys) or absorption (small intestine) and areas of endocrine hormone secretion
allow for increased permeability
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
terminal arteriole
exchange of gases, nutrients, and wastes from surrounding tissue takes place in capillaries
capillary bed
an interwoven network of capillaries between the arterioles and venule
vascular shunt
channel that directly connects arteriole with venule (bypasses true capillaries)
precapillary sphincter
acts as valve regulating blood flow into the capillary bed
blood flow control
arteriole and terminal arteriole dilated when blood needed; constricted to shunt blood away from bed when not needed
veins
carry blood towards the heart
large lumen and thin walls make veins good storage vessels
contains up to 65% of blood supply
venous valves
prevent backflow of blood
most abundant in veins in limbs
venous sinuses
flattened veins with extremely thin walls
varicose veins
dilated and painful veins due to incompetent (leaky) valves
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
blood pressure
force per unit area exerted on the wall of blood vessels by blood
total blood vessel length
longer=more resistance
greatest influence on resistance
blood vessel diameter
relationship between flow, pressure, and resistance
pressure increases=blood flow speeds up
resistance increases=blood flwo decreases
steepest drop in BP occurs where?
arterioles
mean arterial pressure (MAP)
pressure that propels blood to tissues
diastolic pressure + 1/3 pulse pressure (normal=93 mmHg)
muscular pump
contraction of skeletal muscles “milks” blood back toward the heart; valves prevent backflow
respiratory pump
pressure changes during breathing move blood toward the heart by squeezing abdominal veins as thoracic veins expand
sympathetic vasoconstriction
under sympathetic control, smooth muscles constrict, pushing blood back toward heart
capillary BP
ranges from 35 mm Hg at the beginning of the capillary bed to ∼17 mm Hg at the end of the bed
venous BP
small pressure gradient; about 15 mmHg
3 main factors regulating BP
cardiac output, peripheral resistance, blood volume
short term regulation of BP
neural controls (baroreceptors and chemoreceptors) and hormonal controls
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
baroreceptors
pressure sensitive mechanoreceptors that respond to changes in arterial pressure and stretch
vasodilation
decreased CO
chemoreceptors
detect increase in CO2, or drop in pH or O2
cause increased BP by increasing CO or increasing vasoconstriction
hormonal controls
adrenal medulla hormones (epinephrine and norepinephrine), angiotensin 2, ADH, and atrial natriuretic peptide
long term regulation of BP
renal controls alter blood volume via kidneys by direct renal mechanism or indirect renal mechanism
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
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
primary hypertension
90% of cases
no underlying cause identified
no cure but can be controlled
secondary hypertension
less common
due to identifiable disorders
treatment focuses on underlying disorder
orthostatic hypotension
temporary low BP and dizziness when suddenly rising from sitting or reclining position
chronic hypotension
a hint of poor nutrition and warning sign for Addison’s disease or hypothyroidism
acute hypotension
an important sign of circulatory shock
circulatory shock
Condition where blood vessels inadequately fill and cannot circulate blood normally
hypovolemic shock
from large scale blood loss
vascular shock
from extreme vasodilation and decreased peripheral resistance
cardiogenic shock
when an inefficient heart cannot sustain adequate circulation.
