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Exam 3 PE220

Terms in this set (123)

major functions of heart
two seperate pumps, one way pressure gradient, pressure gradient causes blood to flow
major functions of blood vessels
highway for blood, allows blood to be delivered throughout the body

composed of: arteries, veins, and capillaries
major functions of blood
transports oxygen and other nutrients to tissues, carries oxygen and other waste products away from tissues, composed of plasma and formed elements
General composition of blood
half plasma and half red blood cells

bunch of water and erythrocytes
composition of blood plasma.
92% water, 7% proteins, solutes and electrolytes
albumin plasma proteins
liver
-colloid osmotic pressure (keeps it from leaving)
globulin plasma proteins
liver
-lymphoid tissue, clotting factors
fibrinogen plasma proteins
liver
-forms fibrin threads for clotting
transferrin plasma proteins
liver
-other tissues, iron transport
erythrocytes
red blood cells, carry oxygen, biconcave discs
leukocytes
white blood cells, fight infection, irregular shaped
platelets
facilitate clotting, round and oval shape
List the five types of leukocytes
neutrophils, lymphocytes, basophils, monocytes, eosinophils
structure and function of hemoglobin, including its breakdown products.
iron composed of compound in red blood cells, made up of four folded proteins, binds with oxygen

can breakdown into: globin, iron, noniron
hematocrit and state the normal ranges for adult males and females.
proportion of blood made up of red blood cells
males-40-50% women-35-45%
Describe the vascular spasm in hemostasis
immediate constriction of the damaged vessel, triggered by chemicals released from a damaged vessel, decreases blood flow and pressure to damage vessel
role of platelets in hemostasis
platelets adhere to exposed collagen and active and release chemicals
steps involved in the formation of the platelet plug.
1. platelets adhere to exposed collagen and active and release chemicals
2. chemicals cause vasoconstriction and attract more platelets
3. plug forms that seals opening
basic steps of coagulation resulting in the formation of the insoluble fibrin clot.
fibrinogen converted to fibrin, traps red blood cells and more platelets, plug is stabilized, forms a clot (insoluble)
extrinsic factors in hemostasis
caused by external trauma to blood vessels, triggered when tissue factor is exposed and blood escapes, only takes seconds (contact activation)

extrinsic and intrinsic work together to form a clot
intrinsic factors in hemostasis
caused by internal trauma to blood vessels, activated by platelets, proteins, and/epithelium (cell injury)
-takes several minutes
-extrinsic and intrinsic work together to form a clot
explain the role of vitamin K in blood clotting.
vitamin k makes possible for calcium to bind to these factors (calcium needed to activate multiple clotting factors)
-low levels of vitamin k can lead to uncontrolled bleeding
process of fibrinolysis, including the roles of plasminogen, tissue plasminogen activator, and plasmin.
fibrinolysis-removal of clot
-protein called plasminogen converted to plasmin (facilitated by tissue plasminogen activator)
-plasmin breaks down fibrin of clot
Agglutination
clumping of red blood cells
A red blood cell
antibodies B, antigen A
B red blood cell
antibodies A, antigen B
AB red blood cell
no antibodies, A and B antigens
O red blood cell
antibodies A and B, no antigens
Rh factor
presence or lack of antigens on the surface of red blood cells, which causes a reaction between Rh-positive blood and Rh-negative blood

Rh system is considered the most important blood group system after ABO
Blood antigens
Proteins found on the erythrocyte cell surface. Three antigens (A, B, and Rh) are used to differentiate blood groups
Blood antibodies
proteins that attach to opposite blood cell types
Rh positive blood
CAN receive Rh positive and negative blood
Rh negative blood
ONLY receive Rh - Negative blood
Rh factor and pregnancy
only issue if mom is rh- and baby is rh+
if mom is exposed it will cause issues for baby
universal donor blood type
O negative
recipient blood type
AB+
cardiac pacemaker cells
autorhythmic cells, minimal myofilaments, spontaneous

pacemaker potential drift-sodium influx
depolarization- calcium influx
repolarization- potassium efflux
cardiac muscle action potential
consists of rapid deoplarizaton (phase 0), initial rapid repolarization (phase 1), plateua (phase 2), late rapid repol (phase 3), and resting potential (phase 4).

-depolarization begins with Na entering the cell rapidly.
-early repolarization= k channels
-plateau phase where calcium and potassium compete
-repolarization is closure of Ca++ channles and opening of K+ channels.
-resting potential is k channels


action potential duration and refractory period duration is long
skeletal muscle action potential
needs outside input to have an action potential
-depolarization: sodium
-has a resting membrane potential
-has short refractory period and action potential duration
Explain the significance of the plateau phase in the action potential of a cardiac contractile cell.
lengthens time of the action potential, allows for relaxation of heart muscles which allows the ventricles to fill before contraction
arteries
transport blood away from the heart
Capillaries
gas exchange, connection between arteries and veins
veins
Blood vessels that carry blood back to the heart
Trace the path of blood through the right and left sides of the heart, including its passage through the heart valves, and indicate whether the blood is oxygen-rich or oxygen-poor.
vena cava, right atrium, tricuspid valve, right ventricle, pulmonary valve, pulmonary artery, pulmonary capillaries, pulmonary vein, left atrium, bicuspid valve, left ventricle, aortic vein, aorta
List the parts of the electrical conduction system of the heart in the correct sequence for one contraction
sa node, av node, av bundle, right and left bundle branches, Purkinje fibers
SA node
pacemaker, atrial contraction (fires at a high frequency so it sets pace)
AV node
this group of cells is found between the atria and ventricles. It transmits electrical impulses from the atria, where the action potential is briefly delayed as they contract, to the AV bundle.
AV bundle
between the atria and the lower chambers of the heart (the ventricles), allows the movement of the action potential from the septum in the atria to the septum dividing the ventricles
left and right branches
moves signal along
Purkinje fibers
ventricular contraction, begin at the interventricular septum down to the apex of your heart and continue through the myocardium, convey electrical impulses to the ventricles' muscle cells, resulting in a heartbeat
Explain why the SA node normally paces the heart
because it sets the pace of the heartbeat. It is where cardiac muscle contraction begins, from an impulse that causes the right and left atria to contract and push blood into the ventricles
P wave
atrial depolarization (contraction)
QRS complex
ventricular depolarization and atrial repolarization
T wave
ventricular repolarization
PR interval
occurs between onset of p wave and start of QRS complex, delay of AV node to allow filling of ventricles
QT interval
occurs from onset of QRS complex to the end of T wave, ventricular systole
TQ interval
occurs from the end of t wave to beginning of QRS complex, ventricular diastole
RR interval
interval between peak of two successive QRS complexes, time it takes for one cardiac cycle
cardiac cycle
amount of time it takes for the heart to go through systole and diastole

events of cardiac cycle: wiggers, ekg, pressure and volume, heart sound
systole
time it takes for heart to contract (emptying)
diastole
time it takes for heart to relax (filling)
atrial systole
phase of atrial contraction. atrium contracts to pump blood in the ventricles
ejection
t wave, pressure increases then decreases, no heart sounds, semi lunar valve is closed, and volume decreases
isovolumic relaxation
pressure decreases, heart sound is DUB, valves are closed, volume is constant
filling
p wave, pressure increases, no heart sound, AV valve is open, and volume increases
isovolumic contraction
QRS complex, pressure increases, heart sound is LUB, the valves are closed, and volume is constant
systolic blood pressure
pressure in arteries during contraction of left ventricle
-maximal arterial pressure
diastolic blood pressure
pressure during relaxation of left ventricle
-minimum arterial pressure
aortic pressure
120/80 mmHg
Compare and contrast pressure and volume changes of the left and right ventricles during one cardiac cycle.
volume of blood enters and leaves R and L ventricle about same
-Right side: pulmonary circuit
-Left side: systemic circuit

diastolic BP is similar, systolic BP is different (20 vs 120)
Given the heart rate, calculate the length of one cardiac cycle.
60 sec/min divided by HR
Define cardiac output (CO) and state its units of measurement.
the volume of blood pumped from the ventricle in one minute
-liters per minute

cardiac output= stroke volume * HR

stroke volume= end diastolic - end systolic
Predict how changes in heart rate (HR) and/or stroke volume (SV) will affect cardiac output (CO).
if HR increases then SV will decrease to maintain cardiac output (vise versa)
ejection fraction
percent of end diastole volume ejected

SV/EDV*100
cardiac reserve
difference between resting and maximal cardiac output

can be used to determine cardiovascular health
high is good, low is bad
end diastolic volume (EDV)
amount of blood left in ventricle at end of filling or relaxation
end systolic volume (ESV)
amount of blood left in ventricles at end of emptying/contraction
calculate stroke volume (SV) given values for EDV and ESV
EDV-ESV expressed as ml
venous return

plain the factors that affect them
rate at which blood returns to heart
preload
tension on muscle prior to contraction, pressure on walls of left ventricle end at diastole due to EDV
afterload
load against which muscle exerts its force, cardiovascular pressure in aorta at beginning of systole that ventricle must push against to push blood forward
Explain how venous return, preload, and afterload each affect end diastolic volume (EDV), end systolic volume (ESV), and stroke volume (SV).
increasing preload= EDV increases, ESV stays same, SV increases

decreasing preload= EDV decreases, ESV same, SV decreases

increasing afterload= EDV same, ESV increases, SV decreases
State the Frank-Starling Law of the heart and explain its significance.
stretch determines the number of cross bridges, more strength=more force=more SV
Explain the influence of positive and negative inotropic agents on stroke volume (SV).
known as ventricular contractility
force of contraction at given preload

positive increases contraction
negative decreases contraction
Describe the influence of positive and negative chronotropic agents on HR.
chronotropic agents affect how often the heart contracts

positive increases HR (norepi)
negative decreases HR (acetylcholine)
Describe the role of the autonomic nervous system in the regulation of cardiac output.
PNS is no change

SNS response releases norepi onto cardiac muscle cells, which has two effects:
1. increase in calcium permeability during plateau causes the second peak
2. activation of phospholamban (turbo) which creates calcium to go back into SR at a faster rate
-then more calcium=more cross bridges=more force
action potential duration shortens due to turbo
systemic circulation
left heart to body to right heart
-high pressure
-arteries are oxygen rich and veins are oxygen poor
pulmonary circulation
right side of the heart pumps blood to the lungs to left heart
-low pressure
-pulm arteries o2 poor, pulm veins are o2 rich
portal system
begins and ends with capillaries
2 main portal systems: liver and kidneys
hepatic portal system
provide blood to liver that may have toxins
-blood from GI tract is dumped into portal circulation
-blood goes to capillary beds and allows for toxins to go to liver
placenta
where nutrients and gas exchange occurs
ductus venosus
connects the umbilical vein to the inferior vena cava, bypassing the liver

helps get o2 blood to the brain
umbilical vessels
carries oxygenated and nutrient rich blood to the fetus

umbilical vein-o2 rich blood from mom
umbilical arteries-o2 poor blood from fetus
ductus arteriosus
connects the pulmonary artery to the aorta, bypassing the lungs
foramen ovale
opens between r and l atrium, allows blood to bypass lungs and go directly into left heart
Trace the pathway of blood flow from the placenta, through the fetal heart and body, and back to the placenta.
placenta, umbilical vein, ductus venous (liver bypass), inferior vena cava,

right atrium, foramen ovale (bypass lungs) left atrium, aorta, umbilical artery, placenta
or
right ventricle, left ventricle, pulmonary trunk, ductus arteriosus (lungs bypass), aorta, umbilical artery, placenta
fetal circulation bypass
ductus venous= liver
ductus arteriosus, foramen ovale=lungs
Prenatal vs. Postnatal Circulation
umbilical cord is clamped, stops flow of o2 and nutrients from mom, lungs expand, and closes foramen ovale and ductus arteriosus
blood flow (Q)
cardiac output (volume of blood leaving heart per min)

flow=pressure/resistance
blood pressure (change P)
mean arterial pressure (average pressure in systemic circulation)

pressure=flow*resistance
peripheral resistance (R)
resistance in systemic circulation

resistance=pressure/flow
greatest cross-sectional area is
capillaries
lowest pressure is
veins
causes of diastolic and occurs where
elastic recoil of the arteries and occurs in ventricular relaxation
causes of systolic and occurs where
ventricular contraction
peripheral resistance importance
viscosity- thickness of fluid, increase viscosity=greater resistance

vessel length- length of tube, longer tube=greater resistance
pulse pressure
the strength of the pulse wave, defined as the systolic pressure minus the diastolic pressure

low pp= low sv which can be heart failure
high pp= stiff arteries, aortic regurgitation
State the equation relating mean arterial pressure (MAP) to cardiac output (CO) and total peripheral resistance (TPR).
MAP= cardiac output (TPR)
MAP=HRSVTRP
MAP=1/3SBP +2/3DBP

if MAP increases then the other increases
-trp, sv, hr, preload
Explain the mechanisms of capillary exchange of gases, nutrients, and wastes.
primary site of exchange between blood and interstitial fluid, walls are very thin, substances generally move across via diffusion, water moves by filtration and osmosis
hydrostatic pressure
wants to leave, pushing force
osmotic pressure
wants to enter, pulling force
filtration forces
fluid out of capillaries

-interstitial osmotic, capillary hydrostatic
reabsorption forces
fluid going into capillaries

-interstitial hydrostatic, capillary osmotic
Explain how changes in net filtration pressure (NFP) can result in edema and how a functional lymphatic system normally prevents edema.
filtration pressure-absorption pressure
if number is greater than zero then filtration occurs

-high filtration pressure can lead to fluid build up (edema)
-edema is prevented by lymphatic system which keeps fluid moving
vasodilation
widening of blood vessels
vasoconstriction
narrowing of blood vessels
skeletal muscle pump
contraction of muscles and presence of valves, prevents back flow, exercise promotes blood flow back to heart
respiratory pump-inhalation
diaphragm contracts, increase thoracic volume, decrease thoracic pressure, creates pressure gradient, blood flows into r side of lungs and heart, increase pulm blood volume

results in decrease sv
respiratory pump-exhalation
diaphragm relaxes, decreases thoracic volume, increases thoracic pressure, reverses pressure gradient, blood flows into r side of lungs and heart, decrease blood volume

results in increase in sv
baroreceptor reflex and describe how this reflex maintains blood pressure homeostasis when blood pressure changes
baroreceptor- sense pressure via stretch

increase pressure=increase stretch of receptors, more action potential sent to medulla

decrease pressure=decrease stretch of receptors, fewer action potentials sent to medulla
increase PNS and increase BP
increase bp, increase baro stretch, increase firing rate, control center,

-increase release of acetylcholine
-increase binding to muscarinic cholinergic receptors on sa node
-decrease binding to beta adrenergic receptors on as node
1. decrease sa node firing rate
2. decrease hr, decrease cardiac output (decrease binding to beta adren receptors on vent, results in decrease vent contractibility) decrease SBP, decrease MAP
decrease SNS and decrease BP
increase bp, increase baro stretch, increase firing rate, control center,

-decrease release of norepi, epi

norepi
1. decrease binding to beta adrenergic receptors on sa node, decrease sa node firing rate, decrease hr, decrease cardiac output decrease SBP, decrease MAP
2. decrease binding to beta adren receptors on vent, results in decrease vent contractibility, decrease sv, decrease cardiac output, decrease SBP, decrease MAP

epi
-decrease binding to alpha adrenergic receptors on aterials, vasodilation, decrease tpr, decrease dbp, decrease map
hormones in BP
epi- vasoconstriction, increase pressure
noreepi- increase hr, sv increases pressure
angiotensin 2- vasoconstrction, increase pressure
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