Questions Flashcards
What is the number 1 cause of death?
cardiovascular disease
What is the major underlying cause of cardiovascular disease?
ischemia due to atherosclerosis, white thrombus, red thrombus or artery spasm
What is the link to atherogenesis?
high blood cholesterol and inflammatory mechanisms
What characterizes early atherogenesis?
leukocyte recruitment and expression of proinflammatory cytokines
What promotes inflammatory pathways and is responsible for most MIs and strokes?
thrombosis
What can modulate inflammation?
nervous system
Define hemostasis.
prevention of blood loss
What are the mechanisms of hemostasis?
vascular spasm, formation of a platelet plug, blood coagulation, fibrous tissue growth to seal
What is vascular constriction associated with?
trauma
What can cause vascular constriction?
neural reflexes, local myogenic spasm, local humoral factors
What is responsible for most vascular constriction?
local myogenic spasm
What are local humoral factors?
thromboxane A2 from platelets
What type of vascular constriction is important for small blood vessels?
local humoral factors
How does neural reflex work for vascular constriction?
the sympathetic nervous system induces constriction because of pain
True or false: platelets function as whole cells, including being able to divide
False
What do platelets contain?
contractile proteins (actin and myosin), enzymes, calcium, ADP, ATP, thromboxane A2, serotonin and growth factors
What do platelet cell membranes contain?
glycoproteins and phospholipids containing platelet factor 3
What is thromboplastin?
a phospholipid containing platelet factor 3 that initates blood coagulation
What is the mechanism of Platelet Activation when platelets contact damaged area?
1) swell
2) irregular form with irradiating processes protruding from the surface
3) contractile proteins contract causing granule release
4) secrete ADP, Thromboxane A2 and serotonin
What is thromboxane A2?
it is a vasoconstrictor and stimulates platelet degranulation
it also accelerates platelet activation, it is NOT needed to activate
What happens when there aren’t enough platelets in the blood?
are associated with small hemorrhagic areas under the skin and throughout internal tissues
What is the half life of platelets?
8-12 days
How are platelets eliminated?
mostly by macrophage action
What does the endothelial wall produce and prevent?
prevents platelet aggregation
produces prostacyclin (PG12) and factor VIII
What does prostacyclin do?
it is a vasodilator, stimulates platelet adenylcyclase and inhibits platelet degranulation
When platelet adenyl cyclase is activated, what does it do?
supresses release of granules
What is the pathway to create thromboxane A2?
phospholipid –lipase–> ARA –FA cyclooxygenase–> PGG PHG –thromboxane synthetase–> Thromboxane A2
What is the pathway to create prostacyclin?
phospholipid –lipase–> ARA –FA cyclooxygenase–> PGG PHG –prostacyclin synthetase–> prostacyclin
What do aspirin and ibprofen do?
block thromboxane A2 and prostacyclin prodution by blocking FA cyclooxygenase which in turn converts ARA to PGG and PGH (intermediates
Why take aspirin to prevent heart attacks?
to block platelet function
What do anticoagulants do?
prevent clots from forming
How do anticoagulants prevent clots from forming?
they use chelators (tie up calcium), heparin (complexes with antithrombin IIII) and dicumarol (inhibits vitamin K dependent factors
What are the factors that are synthesized by hepatocytes?
II, VII, IX and X
Where are endogenous activators found?
tissues, plasma and urine
What are the exogenous activators of plasminogen?
streptokinase and tissue plasminogen activator
What is reperfusion injury associated with?
formation of highly reactive oxygen species with unpaired electrons
When are free radicals generated?
when pressure on tissues is relieved and again perfused with blood
What is collateralization?
the ability to open up alternate routes of blood flow to compensate for a blocked vessel
What are the types of collateralization?
angiogenesis and vasodilation
What is the role of the sympathetic nervous system on collateralization?
may impede via vasoconstriction, may augment via release of neuropepetide Y
What is the extrinsic mechanism for thrombosis?
initiated by chemical factors released by damaged tissues
What is the intrinsic mechanism for thrombosis?
requires only components in blood and trauma to blood or exposure to collagen
What are the names of the clotting factors we need to know?
fibrinogen, prothrombin, thromboplastin, calcium
What organ is key in clotting?
liver
What are the 5 clotting factors that are synthesized in the liver?
fibrinogen, prothrombin, SPCA, AHF B, stuart factor
What does coumarin do?
depresses liverformation of II, VII, IX and X by blocking action of vitamin K
What is hemophilia?
a sex linked disease that almost exclusively in males
85% of cases have a defect in factor VIII (antihemophilic factor A
15% of cases defect in factor IX (antihemophilic factor B)
Which steps of blood coagulation have calcium?
all but the first two steps
When the extrinsic and intrinsic factors merge, what happens?
it activates factor V and X and prothrombin to thrombin
What is needed to activate factors IX and X?
calcium
What are the final commonsteps of fibrin (polymer)?
fibrinogen + thrombin –> fibrin (monomer) + activated factor XIII
What breaks down the mesh (fibrinogen)?
plasmin
What is antiphospholipid antibody syndrome?
an autoimmune disorder where the body makes antibodies against phospholipids in cell membranes which cause abnormal clots to form
What are some risk factors for heart disease?
increasing age male gender heredity (race included) tobacco smoker high cholesterol high blood pressure physical inactivity obesity/overweight diabetes mellitus high blood homocysteine
What is homocysteine?
an amino acid in the blood that may irritate blood vesels promoting atherosclerosis
it can also cause cholesterol to change into oxidized LDL
itcan make blood mroe likely to clot
high levels of homocystein in the blood can be reduced by increasing folic acid, B6 and B12 in the blood
What are the agglutinogens (surface markers) that are found on each of the blood types?
O- none
A- A
B- B
AB- A and B
What are the agglutins (soluble antibodies) that are found on each of the blood types?
O- anti A and B
A- Anti B
B- Anti A
AB- none
When are agglutinins produced?
after birth, arising spontaneously
When are antibody titers peak?
around 10 years old
Which blood types have anti A sera?
A, AB
Which blood types have anti B sera?
B, AB
Which blood type has neither seras?
O
How does the body lyse RBC when the wrong blood type is given?
antibodies (primarily IgM) cause kysis of RBCs by activating the compliment system which releases proetolytic enzymes rupturing cells membrane
What is the most lethal effect of a transfusion reaction?
kidney failure
Why is kidney failure associated with a transfusion reaction?
toxic substances are released from hemolysed RBCs, which causes circulatory shock, the hemoglobin from lysed RBCs preceipitates and blocks renal tubules
What are the 6 common Rh antigens?
C, D, E, c, d, e
Can a person with D Rh factor have d as well?
no
Which Rh factor is the most common?
D
Whathappens when Rh+ RBCs are infused into a person who has Rh-?
it stimulates the production of anti-Rh antibodies which develop slowly and reach maximum concentrations 2-4 months later
What is Heolytic disease of the newborn?
agglutination and hemolysis of the fetus’ RBCs by the mother’s anti Rh agglutinins, which can cause jaundice in the fetus
How does hemolytic disease of the newborn occur?
the fetus inherits Rh+ from the father and the mother is Rh-
the mother will develop anti Rh agglutinins from exposure to the fetus’ Rh factor.
When do we usually see hemolytic disease of the newborn?
Usually during the second or third pregnancy
What is erythroblastosis fetalis?
when the mother’s agglutinins circulate in the fetus after birth and destroy RBCs, causing anemia
What are some side effects of erythroblastosis fetalis?
bilirubin might precipitate in neurons of the brain causing mental impairment (kernicterus)
this causes enlargement of the liver and spleen of the baby
What is the treatment of erythroblastosis fetalis?
replace the neonate’s blood with rh- blood
How can one prevent erythroblastosis fetalis?
give an Rh immunoglobulin globulin (an anti-D antibody) to the mother at 28-30 weeks of gestation, whcih interferes with the immune response to the D antigen in the fetal RBCs that may cross the placenta and enter mother’s circuation
What do cardiac muscle cells look like?
long, striated and grouped in irregular anastomosing columns with 1-2 centrally located nuclei
What are SA node, AV node and Purkinje fibers generally?
specialized excitatory and conductive muscle fibers
Define syncytium
many acting as one
Why is there a syncytial nature of cardiac muscle?
because of the presence of intercalated discs
this makes low resistance pathways connecting cardiac cells end to end
there are also gap junctions
What is the duration of a cardiac action potential (AP)?
.2-.3 seconds
What are the channels that allow AP in cardiac muscle?
fast Na+
slow Ca2+/Na+
K+
Describe the permeability changes of sodium, calcium and potassium in the cardiac muscle.
Na+ sharp increase at the onset of depolarization, decrease during repolarization
Ca2+ increased during the plateau of the AP, decrease during repolarization
K+ increased during the resting polarized state, decreased at depolarization
When is the conductance for potassium greatest?
during the resting polarized state
What kind of channels does the SA node have? Why?
only slow CA2+/na+ to increase the depolarization time
What kind of channels does the typical cardiac cell have?
both fast Na+ and slowCa2+/Na+ channels
What does tetradotoxin do?
blocks fast Na+ channels selectively changing a fast response into a slow response
What must we also consider when the channels are open?
the concentration gradient, electrical gradient and the membrane permeability
What will ions seek if the ion channels are open?
Nernst equilibrium potential
What is the Nernst equilibrium potential?
when the concentration gradient favoring ion movement in one direction is offset by the electrical gradient
What happens during the resting membrane potential?
fast Na+ and slow Ca2+/Na+ channels are closed and K+ channels are open. Therefore, K+ ions are free to move
When is a stable Er maintained?
when K+ reaches the Nernst equilibrium potential
Is the Na+/K+ pump energy dependent?
yes
Why is the ratio of Na+ and K+ 3:2, respctively?
there is a net loss of one + charge from the interior each cycle, which helps the interior of the cell remain negative
what does the protein pump utilize?
energy from ATP
What binds to and inhibits the Na+/K+ pump?
digitalis
What happens to the cardiac cell membrane protein when the Na+/K+ pump is inhibited?
the function of the exchange protein is reduced and more Ca2+ is allowerd to accumulate in the cardiac cell increases contractile strength
Describe the absolute refractory period.
it is unable to re-stimulate the cardiac cell and occurs during the plateau of the AP
Describe the relative refractory period.
requires a supra-normal stimulus and occurs during repolarization of the AP
Can you stimulate a cardiac cell during absolute refractory period?
no
How would you describe the relative refractory period in a slow response?
the relative refractory period is prolonged and the refractory period is about 25% longer
What is the function of the the AV node and bundle?
to protect the ventricles from supra-ventricular arrhythmias
How do SA nodes have a self excitatory nature?
less negative Er leaky membrane to Na+/Ca2+ only slow Ca2+/Na+ channels operational spontaneously depolarizes at fastest rate contracts feebly
What is different about the AP for an SA node compared to a cardiac cell AP?
the SA node has no stable resting polarized state
What is overdrive suppression?
when you drive a self-excitatory cell at a rate faster than its own inherent rate
What is the mechanism behind overdrive suppression?
increased activity of the Na+/K+ pump creating a more negative Er
What is an example of overdrive suppression normally found in the heart?
the AV node and purkinje system are under overdrive suppression by the SA node
What is the function of the AV node?
delays the wave of depolarization from entering the ventricle, which allows the atria to contract slightly before the ventricles
What can act as an SA node if the SA node isn’t present?
the AV node, but it is slower than the SA node would be
As the heart rate ____, cycle length ____
increases, decreases
Which is higher at resting heart rate: systole or diastole?
diastole
What happens to the duration of systole and diastole as the heart rate increases?
both get shorter, but diastole shortens to a greater extent
When is left coronary artery pressure peaked?
at the beginning of diastole
When is right coronary artery pressure peaked?
in the middle of systole
What happens when there an increase in potassium efflux?
increased heart rate
What happens when there is a decrease in potassium efflux?
decreased heart rate
What happens when there is a decreased influx of Na/Ca?
decreased heart rate
What happens when there is an increased influx of Na/Ca?
heart rate increases
When there is an increase in potassium efflux and an increase in Na/Ca influx, what happens?
there isno net change in the AP
What happens during systole?
isovolumic contraction of the ventricle and ejection of blood
What happens during diastole?
isovolumic relaxation of theventricle, rapid inflow (70-75%), diastasis, and atrial systole (25-30%)
What is end diastolic volume (EDV)?
volume in ventricles at the end of filling
What is end systolic volume (ESV)?
volume in ventricles at the end of ejection
What is stroke volume (SV)?
volume ejected by ventricles
What is the ejection fraction?
% of EDV ejected (SV/EDV X 100%)
normal is 50-60%
If someone had an EDV of 300 and an ESV of 150, what is their ejection fraction? Is this normal?
300 - 150 = 150
150/300 = 50%
Yes, this is a normal ejection fraction
Define preload.
stretch on the wall prior to contraction (proportional to the EDV)
Define afterload.
the changing resistance (impedance) that the heart has to pump against as blood is ejected
What is an A wave?
it is a wave associated with atrial contraction
What is a C wave?
it is a wave associated with ventricular contraction, specifically bulging of AV valves and tugging on atrial muscle)
What is a V wave?
a wave associated with atrial filling
Draw the atrial pressure wave graph created in class and label all of the important points on the graph.
Try to understand exactly what that graph is saying.
What is the function of the valves?
to open with a forward pressure gradient and close with a backward pressure gradient
Give an example of a forward pressure gradient (draw the schematic if necessary).
when the left ventricular pressure is greater than the aortic pressure, the aortic valve is open
Give an example of a backward pressure gradient (draw the schematic if necessary).
when the aortic pressure is greater than the left ventricular pressure, the aortic valve is closed
What is a forward pressure gradient also known as?
systole
What is a backward pressure gradient also known as?
diastole
What is it called when both the aortic and mitral valve are closed and the left ventricular pressure is rising?
isovolumic contraction
What is it called when both aortic and mitral valve are closed and the left ventricular pressure is decreasing?
isovolumic relaxation
What is a jugular pulse?
right atrial pressure release
Describe the mitral and tricuspid valve.
thin and filmy, have corda tendinae that act as check lines to prevent prolapse, have papillary muscles to increase tension on chorda tendinae
Describe the pulmonic and aortic valves.
stronger construction
Define stenosis.
when the valve doesn’t open fully
Define insufficiency when related to valves.
when the valve doesn’t fully close
What is the vibrational noise created by either a stenosis or insufficiency?
murmur
When listening to a patient’s heart, you hear a murmur during diastole. What pathology could they have if there was a problem on the left side of the heart?
mitral stenosis, aortic insufficiency
When listening to a patient’s heart, you hear a murmur duing diastole. What pathology could they have if there was a problem on the right side of the heart?
tricuspid stenosis, pulmonary insufficiency
When listening to a patient’s heart, you hear a murmur during systole. What pathology could they have if there was a problem on the left side of the heart?
mitral insufficiency, aortic stenosis
When listening to a patient’s heart, you hear a murmur during systole. What pathology could they have if there was a problem on the right side of the heart?
tricuspid insufficiency, pulmonary stenosis
At a given operating pressure, as ventricular radius increases, developed wall tension ____?
increases
What happens to the force of the ventricular contraction when the tension is increased?
the force also increases
How does the law of laplace explain how capillaries can withstand high intravascular pressure?
the small radius makes it easier on the vessels so there’s not so much wall tension
Define cronotropic.
anything that affects heart rate
What are some examples of something that could be +cronotropic?
caffeine, NE
Define dromotropic
anything that affects conduction velocity
What are some examples of something that could be + dromotropic?
NE
Define inotropic.
anything that affects the strength of contraction
What is an example of something that could be +inotropic?
caffeine, NE
What is the Frank-Starling Law of the Heart?
within physiologic limits, the heart will pump all the blood that returns to it without allowing excessive damming of blood in the veins
What is the mechanism behind the Frank-Starling Law of the Heart?
increased venous return causes increased stretch of cardiac muscle fibers, which increases cross-bridge formation and increased calcium influx (which both increase the force of the contraction). It also increases the streth on the SA node which increases heart rate
When cardiac fibers are stretched beyond their limit, what happens?
the cross bridges become smaller, the less the cross bridge, the less calcium that can influx
What is homeometric autoregulation?
the ability to increase strength of contraction independent of a length change
During homeometric autoregulation, when is flow induced?
when the increased stroke volume is maintained even as the EDV decreases back to its initial levels (ESV also decreases)
During homeometric autoregulation, when is pressure induced?
when an increase in aortic BP will increase the force of the left ventricular contraction
During homeometric autoregulation, when is rate induced?
when increased heart rate (decreased cycle length) increases force “treppe”
Why can ESV also decrease when flow is induced?
because there is a little blood left over after a contraction, so the ESV can go lower, there will just be less leftover blood
What happens when there is direct stretch on the SA node?
increases calcium and/or sodium permeability which will increase heart rate
What are some extrinsic influcences on the heart?
autonomic nervous system, hormonal influences, ionic influences, temperature influences
When sympathetics control the heart, what is true?
+ cronotropic
+inotropic
+ dronotropic
When parasympathetics control the heart, what is true?
- cronotropic
- inotropic
- dronotropic
How is the SNS blocked from the heart?
with propranolol (a beta blocker) which blocks beta receptors
How is the PSNS blocked from the heart?
with atropine which blocks muscarinic receptors, which with increase heart rate, butdecrease strength of contraction
Parasympathetic NS exerts a _______ _______ influence on heart rate while sympathetic NS exerts a ______ ______ influence.
dominant inhibitory
dominant stimulatory
What accounts for most of the SNS effect on the heart?
direct innervation
What causes indirect effects of the SNS on the heart?
catecholamines (epinephrine, NE) from the adrenal medulla in the blood
When you stimulate the left stellate ganglion of the SNS, what happens to the heart?
decrease in ventricular fibrillation threshold
prolonged QT interval
When you stimulate the right stellate ganglion of the SNS, what happens to the heart?
increased ventricular fibrillation threshold
What is the cardioaccelerator reflex?
when there is stretch on the right atrial wall that increases stretch receptors which in turn send signals to the MO and increase SNS outflow to the heart
What is the purpose of the cardioaccelerator reflex?
to prevent damming of blood in the heart and central veins
What is the benzold-Jarisch reflex?
stimulation of the sensory endings mainly in the ventricles that reflex via CN X to the CNS
What is the Benzold-Jarisch reflex stimulated by?
occlusion of the circumflex artery
increase in left ventricular pressure and left ventricular volume (like in aortic stenosis)
What do thyroid hormones do to the heart?
+ inotropic
+ chronotropic
causes an increase in CO by increasing basal metabolic rate
What is the effect of increased potassium on the heart?
dilation and flaccidity of the cardiac muscle at concentrations 2-3X normal
decreases resting membrane potential
What is the effect of increased calcium on the heart?
spastic contraction
What does the Benzold-Jarisch reflex result in?
hypotension and bradycardia (which would eventually cause you to pass out)
Norepinephrine has an affinity for what?
alpha and beta receptors
Epinephrine has an affinity for what?
beta receptors
What happens when the body has a fever?
heart rate increases about 10 beats for every degree F elevation in body temperature
the contractile strength will increase temporarily but prolonged fever can decrease contractile strength dueto exhaustion of metabolic systems
What happens when the body’s temperature is decreased?
the heart rate and strength decrease
What is the preferred energy substrate for the heart?
FA
What are the other energy sources the heart can use?
glucose, glycerol, lactate, pyruvate, amino acids
How much energy the heart uses is turned into heat?
75%
What is the other 25% of the energy used for?
pressurization of the blood (99%), acceleration of blood (1%)
What kind of energy is pressurization of the blood?
potential energy
What is pressurization of the blood?
moving blood from low pressure to high pressure
What kind of energy is acceleration to the blood’s ejection velocity?
kinetic
What does an EKG measure?
potential difference across the surface of the myocardium with respect to time
What is the lead?
a pair of electrodes
What is the axis of the lead?
line of connecting leads
What is the transition line?
line perpendicular to the axis of the lead
Where can leads be placed on the body?
right arm, left arm
right arm, left leg
left arm, left leg
Which lead is always negative? Positive? Both?
negative= Right arm positive= left leg both= left arm
What does the P stand for in an EKG?
SA and atrial node depolarization
What does the QRS stand for in an EKG?
ventricular depolarization (atrial repolarization is covered up by this)
What does the T stand for in an EKG?
ventricular repolarization
What is PR in an EKG?
the start of atrial and ventricular depolarization
the AV node causes the atrial and ventricular contractions to happen separately
1 mm on an EKG is equal to how much time?
0.04 seconds
What is the time frame for a healthy PR interval?
0.16 seconds
What if the PR interval is greater than 0.20 seconds?
there is a first degree AV block
What is the PR inteval is less than 0.10 seconds?
there is an inadequate delay possible from the accessory conduction pathway from atria to ventricle
What makes an electrode positive or negative?
the deflection is based on what the active electrode sees relative to the reference electrode
In a bipolar limb lead, the leads are connected to which body parts in lead I, II, and III?
I- left arm, right arm
II- left leg, right arm
III- left leg, left arm
The wave of depolarization is moving toward the positive electrode. What happens to the deflection?
increased deflection
The wave of repolarization is moving toward the negative electrode. What happens to the deflection?
increased deflection
The wave of depolarization is moving toward the negative electrode. What happens to the deflection?
decreased deflection
The wave of repolarization is moving toward the positive electrode. What happens to the deflection?
decreased deflection
With a unipolar limb lead, what is positive and what is negative in an AvR?
+ right arm, - left arm and left leg
With a unipolar limb lead, what is positive and what is negative with an AvL?
+ left arm, - right arm and left leg
With a unipolar limb lead, what is positive and what is negative with an AvF?
+ left leg, -left arm and right arm
Where do we place positive electrodes specifically?
V1- intercostal space, right sternal border
V2- 4th intercostal space, left sternal border
V3 equidistant between V2 and V4
V4 5th intercostal space, mid clavicular line
V5 equidistant between V4 and V6
V6 left midaxillary line
Where is the negative electrode?
all limb electrodes hooked together
What do we analyze in an EKG?
rate, rhythm and intervals, axis, hypertrophy, infarction
Draw out the chart that we learned in class for heart rate
MM 5 10 15 20 25 30
sec .2 .4 .6 .8 1.0 1.2
HR 300 150 100 75 60 50
What is the PR inteval?
time from SA node to entering the ventricle and includes AV nodal delay
What can happen with a prolonged QT interval?
increased incidence of sudden caridac death
high propensity to develop ventricular fibrillation
Describe a sinus arrhythmia
longest and shortest RR vary by .16 sec
heart rate variability
What is a 1st degree AV block?
depolarization wave from atria to ventircle is delayed excessively (PR interval > 2 seconds
What is a second degree AV block?
some depolarization waves pass, others blocked
dropped beat- P wave with no associated QRS complex
What is a thrid AV block?
all depolarization waves from atria to ventricles are blocked
no relationship between P waves and QRS waves
How long should a normal QRS complex last?
between .06 and .08 seconds
a prolonged one would be greater than .12 seconds
What is a prolonged QRS wave associated with?
ventricularhypertrophy or conduction block in purkinje system
What is the mean electrical axis??
the average of ventircular depolarization
How does the ventricle depolarize?
from base to apex and from endocardium to epicardium ADIO
What is the range for a normal axis?
-30 to 105 degrees
What does it mean when there is an axis deviation?
conduction block and hypertrophy shift axis to the side of the problem (ex: left bundle branch block creating a left axis deviation
What can cause hypertrophy of a ventricle?
anything that creates an abnormally high work load on that chamber
What blood vessels is the myocardium supplied by?
coronary arteries and their branches
Where else can cells of the heart receive blood?
chamber blood (endocardial cells only)
When does the myocardium take the max oxygen out of the perfusing coronary flow?
resting HR (70% extraction rate
Any ___ demand must be met by ___ coronary flow
increase, increase
What can ischemia do to the depolarization and repolarization of the heart?
prolong depolarization and therefore delay repolarization, which can cause the waves to go in the same direction, which causes an inversion of the T wave
What do damaged cells lose the ability to do?
repolarize
When does damage to heart muscle occur and what is it associated with ?
damage occurs upon reperfusion and is associated with free radical damage
How do you determine if MEA is normal?
If the QRS of lead I and AvF is positive
What limits myocardial blood flow, especially in the left ventricle?
Contraction of cardiac muscle
