heart Flashcards
murmur
sound of blood flowing through a valve
mitral valve stenosis
narrowing of a valve due to Ca2+ deposits or endocarditis
leads to impaired BF from left atrium to left ventricle
increased generated force leads to left atrium hypertrophy and enlargement
treated via BB, CCB, surgery
symptoms include DOE, fatigue, loud S1, mid-diastolic murmur
mitral valve prolapse
blood backflows into the mitral valve and back into the left atrium
reduces CO
may cause pulmonary hypertension
ischemia
heart is deprived of O2
leads to anaerobic respiration and lactic acid buildup
high Ca2+ and H+ conc.
can lead to mitochondria damage and closing of gap junctions
anoxia
deficiency or complete loss of O2 in other tissues of the body
angina pectoralis
chest pain
treated via nitroglycerin (vasodilator), BB, ballon angioplasty/stents
myocardial infraction
aka “heart attack”
Bf to the heart is stopped can be diagnosed via EKG, blood tests, angiogram, echocardiogram
treated via asprin, plavix, BB, surgery
CHF
heart has reduced ability to pump blood
long-term condition
can cause edema to the lower portions of the body
risk factors of myocardial infraction and angina pectoralis
hypertension
dyslipidemia
smoking
P-Q interval
time it takes atria to depolarize
Q-T interval
time it takes ventricles to depolarize and repolarize
flutter
rapid, regular contractions that can later progress to fibrillation
fibrillation
rapid, irregular contractions that can impair pumping of blood and cease circulation
can lead to brain death
heart block
few, or no impulses reach the ventricles, causing them to contract slowly
ventricular filling
mid-late diastole
AV valves open and ventricles start filling w/ blood due to the atria contracting
when pressure of the ventricles exceed the atria the AV valves close
isovolumetric contraction
ventricular systole
all valves closed
volume of blood stays the same
atria relax
ventricles contract
increase in pressure
ventricular ejection
when the pressure in the ventricle exceeds the pressure in the aorta and pulmonary arteries ventricular ejection occurs
isovolumetric relaxation
early diastole
SL valves close
pressure decreases
CO
amount of blood the. heart pumps in 1 min
HR*SV
SV
amount of blood pumped out of one ventricle w/ each beat
EDV-ESV
frank-sterling law
increase in stretch of the heart-> increases contraction size-> increases CO
increase in EDV leads to increase in SV
fibrous pericardium
protects
anchors to surrounding structures
prevents overfilling
myocardium
made up of spiral bundles of contractile cardiac muscle cells and a cardiac skeleton which had interlacing layers of CT
endocardium
made of simple squamous epithelium
continuous w/ the endothelial linings of blood vessels and lines heart chambers and the cardiac skeleton of valves as well
cardiac skeleton
anchor cardiac muscle fibers
support vessels and valves
limit the spread of APs to specific paths
left coronary artery
receive blood from aortic SL valve
branches into circumflex, left marginal, and LAD arteries
right coronary artery
receives blood from pulmonary SL valve
branches into right marginal and PAD arteries
incompetent valve
blood backflows so heart repumps same blood over and over
valvular stenosis
stiff flaps-> constrict opening
heart must exert more force to pump blood
cardiac tamponade
excess fluid sometimes compresses heart->limits pumping ability
col pulmonale
enlargement of the right ventricle
due to increased BP in pulmonary circuit
hypocalcemia
depresses heart
hypercalcemia
increased HR and contractility
hyperkalemia
alters electrical activity
can lead to heart block and cardiac arrest
hypokalemia
feeble heartbeat
arrhythmias
pulmonary congestion
left side fails
blood backs up into lungs
peripheral congestion
right side fails
blood pools in body organs
leads to edema
treatment for pulmonary and peripheral congestion
diuretics
vasodilators
digitalis
coronary sinus
branches into great, middle, and small cardiac veins
empties into right atrium
preload
degree of stretch of cardiac muscle cells before they contract
measures by EDV
contractility
contractile strength
afterload
pressure ventricles must overcome to eject blood
hypertension increases after load
female HR
faster than males
desmosomes
prevent cells from separating during contraction
inotrophic effect
affects contractility
due to medications
can be positive or negative
chronotrophic effect
affects HR
positive or negative
due to SNS or PNS
pericarditis
inflammation of pericardium
creaking sound heard w/ stethoscope (pericardial friction rub)-> roughens membrane surface
HR effect on SV
increase in HR leads to the decrease in EDV, SV, and contractility because there is less time for ventricular filling
VR effect on SV
increase in VR leads to the increase in SV and EDV
BV effect on SV and CO
decrease in BV leads to a decrease in EDV and SV
no change in CO
dicrotic notch
increase in aortic pressure due to blood rebounding against closed SL valve
occurs during isovolumetric relaxation
short-term mechanisms for regulating BP regulate
vessel diameter
HR
contractility
increased resistance
decrease BF
increase BP
increased length
decrease BF
increase BP
increased diameter
increase BF
decrease BP
increased viscosity
decrease BF
increase BP
BP
force of blood pushing against walls of arteries
systolic pressure
pressure exerted in aorta during ventricular contraction
diastolic pressure
lowest level of aortic pressure
pulse pressure
difference b/w systolic and diastolic pressure
pulse
throbbing of arteries
MAP
pressure that propels blood to tissues
diastolic pressure+1/3(pulse pressure)
OR 1/3 systolic + 2/3 diastolic
vaso vasorum
part of large arteries and veins that nourish tunica externa
precapillary spinchters
regulate BF into true capillaries
veins
contain venous valves and venous sinuses
formed when venules converge
lower BP than arteries
act as blood reservoirs
large diameter
little resistance
contain up to 65% of blood supply
venous valves
prevent backflow of blood
venous sinuses
flattened veins w/ extremely thin walls (coronary sinus of heart)
long-term renal regulation
alters BV
direct renal mechanism
elimination of urine (decreases BP)
conservation of water (increases BP)
indirect renal mechanism
RAAS
renin converts angiotensinogen into angiotensin I in liver-> angiotensin I converted to angiotensin II via ACE in lungs
angiotensin II
releases aldosterone and ADH
increases thirst
stimulates vasoconstriction
increases BP
muscular pump
milks blood towards the heart due to contraction of skeletal muscle
respiratory pump
moves blood towards the heart by squeezing abdominal veins as thoracic veins expand in response to pressure changes during breathing
venoconstriction
pushes blood towards the heart under sympathetic control
tunica intima
slick surface
reduces friction
elastic fibers
simple squamous epithelium
tunica media
made up of SM and sheets of elastin
control vasoconstriction and vasodilation
influence BF and BP
tunica externa
made up of collagen fibers
protect, reinforce, and anchor to surrounding structures
contains nerve fibers and lymphatic vessels
elastic arteries
contain elastin
large lumen
low resistance
acts as pressure reservoir
inactive in vasoconstriction
ex. aorta
muscular arteries
distal to elastic arteries
deliver blood to organs
active in vasoconstriction
arterioles
smallest arteries
lead to capillary beds
control flow via vasocontriction and vasodilation
most resistance
capillaries
smallest blood vessels
pericytes= help stabilize walls and control permeability
exchange gases, nutrients, wastes, and hormones b/w blood and ISF
continuous capillaries
abundant in skin and muscle cells
help form BBB in brain
rich in tight junctions
fenestrated capillaries
more permeable than continuous capillaries
contain pores
found in small intestine, endocrine glands, and kidneys
function is absorption and filtrate formation
sinusoid capillaries
fenestrated
few tight junctions
found only in the liver, bone marrow, spleen, and adrenal medulla
contain macrophages in linings
venules
formed when capillary beds unite
very porous
secondary hypertension
due to issues in the kidneys, hyperthyroidism, and cushing’s syndrome
blood flow
fastest in the aorta
slowest in capillaries
vasomotion
slow, intermittent flow
reflects on/off opening and closing of precapillary sphincters
HPc
force fluids through capillary walls
35 mm Hg at arterial end
17 mm Hg at venous end
filtration occurs at arterial end
HPif
pressure that would push fluid into vessel
0 mm Hg
OPc
nondiffusible plasma proteins draw water towards themselves (pulls water into capillary)
26 mm Hg
absorption occurs at venous end
OPif
1 mm Hg
increases as fluid leaves the capillaries and enter IF
NFP
comprises all forces acting on capillary bed
NFP=(HPc+OPif)-(HPi+OPc)
celiac trunk
comprised of left gastric, splenic, and common hepatic arteries
hepatic portal vein
drains into splenic, gastric, superior and inferior mesenteric veins
atherosclerosis
arteries harden or thicken due to plaque build up
arteriosclerosis
arteries gradually harden and become damaged
aneurysm
abnormal buldge or ballooning in the wall of a blood vessel
circulatory shock
any condition in which blood vessels inadequately fill and blood cannot circulate normally
results in inadequate blood flow to meet tissue needs (hypoxia)
hypovolemic shock
results from large-scale blood loss
vascular shock
results for extreme vasodilation and decreased peripheral resistance
cardiogenic shock
results when an insufficient heart cannot sustain adequate circulation (decreased CO)
fetal circulatory system
umbilical vein->ductus venosus (liver)–>foramen ovale (heart) OR ductus arteriosus (heart)->umbillical artery
ductus venosus
allows highly oxygenated blood to bypass liver to the inferior vena cava
foramen ovale
allows blood to bypass lungs and moves blood from the right atrium to the left atrium->left ventricle-> aorta-> aortic arch->umbilical arteries
ductus arteriosus
moves blood from the pulmonary artery to the aorta->aortic arch->umbilical arteries
intercalated discs
two cardiac muscle cells connected by desmosomes and gap junctions
why is the left side of the heart thicker than the right?
increased resistance
increase in pH
leads to vasoconstriction
decrease in pH
leads to vasodilation
myogenic control
ability of SM to respond to changes in mechanical load or intravascular pressure
ADH
water reabsorption
increase BP
aldosterone
sodium reabsorption
increase BP
pectinate muscles
found in atrium
